Judging from what we know about vitamin D, it is highly probable that it confers substantial protection from viral infections, including swine flu.

Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) first connected the dots, identifying the possibility of an influence of vitamin D on incidence of flu.

In 2006, Dr. Cannell reports noticing that the patients in his psychiatric ward in northern California were completely spared from the influenza epidemic of that year, while plenty of patients in adjacent wards were coming down with flu. Dr. Cannell proposed that the apparent immunity to flu in his patients may have been due to the modest dose of 2000 units vitamin D per day he had prescribed that the patients in other wards had not been given. (Since the hospital was run by the state of California, Dr. Cannell apparently had only so much leeway with vitamin D dosing.) While it’s not proof, it’s nonetheless a fascinating and compelling observation.

A similar conclusion was reached in a recent analysis of the National Health and Nutrition Examination Survey demonstrating that the higher the vitamin D blood level, the less likely respiratory infections were.

Personally, I used to suffer through 2 or 3 episodes of a runny nose, sore throat, hacking cough, fevers and feeling crumby every winter. Over the last 3 years since I’ve supplemented vitamin D, I haven’t been sick even once. The past two years I didn’t bother with the flu vaccine, since I suspected that my immunity had been heightened: no flu either winter.

And so it has been with the majority of my patients. Since I began having patients supplement vitamin D to achieve normal blood levels (we aim for 60-70 ng/ml), viral and bacterial infections have become rare.

New research is uncovering myriad new ways that vitamin D enhances natural immune responses to numerous infections, including tuberculosis, bacteria such as those causing periodontal disease and lung infections, and viruses like the influenza virus. Enhanced immunity against cancer is also an intensive area of research on vitamin D.

Will vitamin D supplementation sufficient to achieve desirable blood levels confer sufficient immunity to swine flu should it come to your door? From what we know and what we’ve seen in the few years of vitamin D experience, I think it will in the majority. But I do believe that we should still heed public health warnings to avoid contact with others, minimize exposure to crowds, avoid travel to affected areas, etc.

The results of the latest Heart Scan Blog poll are in.

The question: How has your LDL been measured? The 187 responses broke down as:

I have only had a conventional calculated value
108 (57%)

NMR LDL particle number
35 (18%)

Apoprotein B
21 (11%)

Direct LDL cholesterol
21 (11%)

Non-HDL cholesterol
8 (4%)

I don't know what you're talking about
23 (12%)

Remember the TV game show, To Tell the Truth? Celebrities would have to guess which of three guests represented the real person, such as the notorious con man, Frank Abagnale, Jr., or Mad Magazine publisher, William M. Gaines (who stumped celebrity Kitty Carlisle, heard to exclaim, "I never figured it was him. I mean look at the way he's dressed. I was looking for someone who ran a very successful magazine, so I thought it couldn't be him!")

The celebrities playing the game were permitted to ask the three guests a series of questions, hoping to discern who was the real person vs. the two impostors. At the end, each celebrity had to guess who was truly the person of interest. "Will the real Frank Abagnale, Jr. please stand up!"

If we were to act as the celebrities in our LDL game, we quickly discover some telling facts:

--Conventional LDL cholesterol (the only value 57% of our poll respondents have had) is calculated, not measured. LDL is calculated using the 40-year old Friedewald calculation.

--Directly measured LDL cholesterol (the value 11% of respondents had) is just that: directly measured. It eliminates some of the uncertainties of calculated LDL.

--Apoprotein B-Every LDL and VLDL particle produced by the liver contains one apoprotein B molecule. ApoB therefore provides a crude particle count measure of LDL and VLDL particles. Of course, it includes VLDL and is not completely the same as just an LDL measure. Some lipid authorities Like Dr. Peter Kwiterovich have advocated that apoB replace calculated LDL, and that calculated LDL essentially be discarded.

--Non-HDL cholesterol--I mention this more for completeness. Hardly anybody uses this crude value in practice--Indeed, only 4% of our poll respondents had this measure/calculation. Non-HDL is simply total cholesterol minus HDL cholesterol = Non-HDL cholesterol. It is thus a combination of cholesterol in LDL and VLDL (triglycerides), similar to apoprotein B. While, like apoB, it is a bit different in that it includes VLDL, it has proven a superior measure of risk.

--LDL particle number--In my view, this is the gold standard for LDL and risk measurement, obtained by only 18% of our poll respondents. LDL particle number is proving superior for discriminating who is truly at risk for a cardiovascular event, particularly when metabolic syndrome or diabetes is part of the picture, i.e., when HDL and triglycerides are considerably distorted, leading to substantial corruption of calculated LDL.

While 18% is a minority, it still represents growth in recognition that conventional calculated LDL cholesterol is an unreliable, inaccurate, and outdated value. If the real LDL were to stand up, I believe that it is LDL particle number that would spring to its feet.

We already know that vitamin D reduces inflammatory processes, since several markers, including c-reactive protein and IL-6 have previously been shown to drop substantially with vitamin D. Inflammation underlies coronary atherosclerotic plaque growth, as well as plaque rupture that triggers heart attack.

A German group has now shown that the important inflammatory marker, tumor necrosis factor (TNF), is also reduced by vitamin D supplementation. Many studies have implicated increased TNF levels in promoting cancer.

In this study, a modest vitamin D dose of 3320 units (83 micrograms) was given vs. placebo. The 25-hydroxy D level reached in the treated group was 34.2 ng/ml (85.5 nmol/L), which resulted in a 26.5% reduction in TNF compared with 18.7% reduction (?) in the placebo group.

Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers.

Zitterman A, Frisch S et al.

BACKGROUND: High blood concentrations of parathyroid hormone and low concentrations of the vitamin D metabolites 25-hydroxyvitamin D [25(OH)D] and calcitriol are considered new cardiovascular disease risk markers. However, there is also evidence that calcitriol increases lipogenesis and decreases lipolysis.
OBJECTIVE: We investigated the effect of vitamin D on weight loss and traditional and nontraditional cardiovascular disease risk markers in overweight subjects.
DESIGN: Healthy overweight subjects (n = 200) with mean 25(OH)D concentrations of 30 nmol/L (12 ng/mL) received vitamin D (83 microg/d) or placebo in a double-blind manner for 12 mo while participating in a weight-reduction program.
RESULTS: Weight loss was not affected significantly by vitamin D supplementation (-5.7 +/- 5.8 kg) or placebo (-6.4 +/- 5.6 kg). However, mean 25(OH)D and calcitriol concentrations increased by 55.5 nmol/L and 40.0 pmol/L, respectively, in the vitamin D group but by only 11.8 nmol/L and 9.3 pmol/L, respectively, in the placebo group.

(Calcitriol = 1,25-dihydroxy vitamin D.)

Knowing your vitamin D blood level is crucial, as individual need for vitamin D varies widely from one person to the next. You can get your vitamin D tested at home by going to Grassroots Health or the Track Your Plaque Marketplace.

It all started back in the 1960s, when ape-watching anthropologists, Drs. Jane Goodall and Richard Wrangham, observed chimps foraging for a specific variety of leaf, which they consumed whole while wrinkling their noses in presumed disgust. Subsequent study showed that the leaves contained a powerful anti-parasitic compound.

A similar observation followed in 1987 by Dr. Michael Huffman from the University of Kyoto. During his year of living in the jungles of Tanzania, he observed chimpanzees in their native habitat. On one unexpected morning, he observed a female chimp, Chausiku:

“Chausiku goes directly to and sits down in front of a shrub and pulls down several new growth branches about the diameter of my little finger. She places them all on her lap and removes the bark and leaves of the first branch to expose the succulent inner pith. She then bites off small portions and chews on each for several seconds at a time. By doing this, she makes a conspicuous sucking sound as she extracts and swallows the juice, spitting out most of the remaining fiber. This continues for 17 minutes, with short breaks as she consumes the pith of each branch in the same manner.”

Dr. Michael Huffman’s description of Chausiku documents a fascinating example of animal self-medication what some call "zoopharmacognosy."
In this instance, the chimpanzee, weak, clutching her back in pain, and listless, was ingesting the leaves of the plant, Vernonia amygdalina, to purge an intestinal parasite. She recovered by the next morning.

Vernonia leaves have since been found to contain over a dozen potential anti-parasitic compounds. Chimps in this region commonly suffer infestations of parasites like Strongyloides fuelleborni (thread worm), Trichuris trichiura (whip worm), and Oesophagostomum stephanostomum (nodular worm). They have somehow stumbled onto a treatment that they administer themselves.

Chimpanzees have inhabited earth for over 6 million years. Who knows how long they and other primates have practiced some form of self-medication.

If chimpanzees can do it, I believe that we, as human primates, can also practice a similar form of self-directed health--homopharmacognosy?

Image courtesy Wikipedia

In honor of Earth Day, I thought I'd highlight the unexpectedly high carbon costs of activities in hospitals, specifically the cardiac catheterization laboratory.

A patient enters the cath lab. The groin is shaved using a plastic disposable razor, the site cleaned with a plastic sponge, then the site draped with an 8 ft by 5 ft composite paper and plastic material (to replace the old-fashioned, reusable cloth drapes). A multitude of plastic supplies are loaded onto the utility table, including plastic sheaths to insert into the femoral artery (which comes equipped with a plastic inner cannula and plastic stopcock), a multi-stopcock manifold that allows selective entry or removal of fluids through the sheath, a plastic syringe to inject x-ray dye, plastic tubing to connect all the devices (total of about 5 feet), and multiple plastic catheters (3 for a standard diagnostic catheterization, more if unusual arterial anatomy is encountered).

All these various pieces come packed in elaborate plastic (polyethylene terephthalate or other polymers) containers, which also come encased in cardboard packaging.

Should angioplasty, stenting, or similar procedure be undertaken, then more catheters are required, such as the plastic "guide" catheters that contain a larger internal lumen to allow passage of angioplasty equipment. An additional quantity of tubing is added to the manifold and stopcock apparatus, as well as a plastic Tuohy-Borst valve to permit rapid entry and exit of various devices into the sheath.

Several new packages of cardboard and plastic are opened which contain the angioplasty balloon, packaging which is usually about 4 feet in length. The stent likewise comes packaged in an 18-inch or so long package with its own elaborate cardboard and plastic housing.

At the conclusion of the procedure, another cardboard/plastic package is opened, this one containing the closure device consisting of several pieces of plastic tubes and tabs.

If the procedure is complicated, the number of catheters and devices used can quickly multiply several-fold.

By the conclusion of the procedure, there are usually two large, industrial-sized trash bins packed full of cardboard, plastic packaging, and discarded tubing and catheters. The trash is so plentiful that it is emptied following each and every procedure. None of it is recycled, given the contamination with human body fluids.

That's just one procedure. The amount of trash generated by these procedures is staggering, much of it plastic. I don't know how much of the U.S.'s annual plastic trash burden of 62 billion pounds (source: EPA) originates from the the cath lab, but I suspect it is a big number in total.

So if you are truly interested in reducing your carbon footprint and doing your part to be "green," avoid a trip (or many) to the cath lab.

What if the system to provide heart care has already gotten as big as it should be?

Worse (for hospitals), what if it’s already far larger than it needs to be? Can the system continue to increase revenues if they’ve already attained titanic proportions and outgrown demand? After all, darn it, there are only so many sick people around.

Hospital administrators might have to face an unpleasant choice: downsize to strip excess capacity and suffer the consequences in a competitive market, or . . . fabricate demand for their services.

Like the Dustin Hoffman and Robert DeNiro characters in the movie, Wag the Dog, about how two media-manipulators divert public attention away from a Presidential sex scandal by fabricating a war, spin is everything. It’s enough to sidetrack public attention from a scandal, obscure a truth, send us on a useless detour.

If healthcare for the heart isn’t driven by need, but many still desire to reap the benefits of the procedure-focused system, why not increase the perceived need?

That’s precisely the course that many hospital systems have chosen to follow. If the market you serve has been tapped to its full potential, then grow the market.

Imagine if a company like General Motors were to operate this way. In 2006, for instance, GM sold 9.1 million automobiles. If GM executives were to decide that they’d like to outstrip Toyota by boosting sales by 10% to 10 million, how would they do it? They would first have to determine whether it was feasible to grow demand for their product. If deemed possible, the company would need to ramp up manufacturing capacity to anticipate increased demand. If they miscalculate, GM could be stuck with a costly surplus and have to swallow the costs, maybe selling leftovers at a loss. (We don’t mean to pick specifically on GM; they’re a fine company as far as we’re concerned. This is just a hypothetical illustration.)

But what if a company could concoct some sort of scheme to persuade the car-buying public that they just had to have their cars or trucks? In other words, they could, in effect, create demand for their products.

As perverse as it sounds, that is exactly what occurs in healthcare for heart disease. The system long ago exceeded the necessary level of infrastructure to maintain a high-quality level of care accessible to most Americans. Instead, it continues to grow through a distortion of perception, delivering more services of increasing complexity to larger and larger numbers of people.

The size of the market is therefore a manipulable thing, something that can be massaged and cultivated. There are a variety of clever ways to exaggerate the need for heart procedures.

Why not raise the alarm for heart disease every chance you get? When a local sports figure survived a heart attack here in Milwaukee, St. _____ marketing department was right there, broadcasting the process in TV ads after his recovery. What could be more American than baseball, apple pie . . . and St. _____ Hospital? After his hospital discharge, the 57-year old local icon was shown on the sidelines with his team, back on the job, and at home with family, all beaming, just three months after a bypass operation. “I received only the very best care at St. _____ Hospital. They treated me like family. St. _____ doctors and nurses are the best!” Predictably, a two-month long spike in hospital testing followed filled with people worried whether they, too, might be in imminent danger. Several local cardiologists boasted of the many sports figures who came through the stress testing and heart catheterization labs, though virtually all checked out to be fine.

Though it can serve a legitimate purpose in some situations, stress tests are the ultimate example of a heart scam built on the perception of danger. Pull people in with promises of reassuring them whether or not they have heart disease, only to provide murky results that usually do no such thing. The pitfalls of the test are turned to advantage. The all too common equivocal or mildly abnormal result can be converted into a hospital procedure. (Imagine you could perform such alchemy on the uncertain calculations on your income taxes.)

With millions of stress tests performed every year and the push to perform more and more screening tests, the market has, in effect, been expanded—even though no increase in the disease itself has actually occurred.

Beware: As the scramble for heart patients intensifies, you are going to feel like you are being pulled closer and closer into the jaws of this hungry monster called the American cardiovascular healthcare machine.

There are only two books on heart scans available.

One, of course, is Track Your Plaque.

The other is the basic book on heart scans, What Does My Heart Scan Show?

Lost in the navigation column to the left on this blog is the link to get the electronic version of the book. In case you didn't know, we make this available for free.

If you're interested, just go here. This book can provide many basic answers to the questions that often arise regarding heart scans, such as the expected rate of increase in score, how your score compares to other people, when should a stress test be considered. Many heart scan centers use this book for educational purposes to help patients understand the importance of their heart scan scores.

(The sign-up for the book requires that an e-mail address be entered.)

The hard copy of What Does My Heart Scan Show? is available from Amazon, also, for $12.99.

In the last Heart Scan Blog post, I discussed the question of whether statin drugs provide incremental benefit when excellent lipid values are already achieved without drugs.

But I admit that I was guilty of oversimplification.

One peculiar phenomenon is that, when plaque-causing small LDL particles are reduced or eliminated and leave relatively benign large LDL particles in their place, conventional calculated LDL overestimates true LDL.

In other words, eliminate wheat from your diet, lose 25 lbs. Small LDL is reduced as a result, leaving large LDL. Now the LDL cholesterol from your doctor's office overestimates the true value.

Anne raised this issue in her comment on the discussion:

I eliminated wheat - and all grains - from my diet nearly three years ago (I eat low carb Paleo). My fish oils give me a total of 1680 mg EPA and DHA per day, and my vitamin D levels since last year have varied between 50 ng/ml and 80 ng/ml. However, my lipid profile is not like either John's or Sam's:

LDL cholesterol 154 mg/dl
HDL cholesterol 93 mg/dl
Triglycerides 36 mg/dl
Total cholesterol 255 mg/dl

My cardiologist and endocrinologist are happy with my profile because they say the ratios are good, no one is asking me to take a statin. My calcium score is 0.

However, if we were to measure LDL, not just calculate it from the miserably inaccurate Friedewald equation, we would likely discover that her true LDL is far lower, certainly <100 mg/dl. (My preferred method is the bull's eye accurate NMR LDL particle number; alternatives include apoprotein B, the main apoprotein on LDL.)

So Anne, don't despair. You are yet another victim of the misleading inaccuracy of standard LDL cholesterol determination, a number that I believe should no longer be used at all, but eliminated. Unfortunately, it would further confuse your poor primary care doctor or cardiologist, who--still believe in the sanctity of LDL cholesterol.

By the way, the so-called "ratios" (i.e., total cholesterol to HDL and the like) are absurd notions of risk. Take weak statistical predictors, manipulate them, and try to squeeze better predictive value out of them. This is no better than suggesting that, since you've installed new brakes on your car, you no longer are at risk for a car accident. It may reduce risk, but there are too many other variables that have nothing to do with your new brakes. Likewise cholesterol ratios.

Despite all the hoopla heart disease receives in the media, I continue to marvel at how many people I meet who still think that aspirin, Lipitor, and a low-fat diet constitute an effective heart attack prevention program.

It doesn't. No more than washing your hands prevents all human infections. It helps, but it is a sad substitute for a real prevention program.

Of course, aspirin, Lipitor, and a low-fat diet is the same recipe followed by the unfortunate Tim Russert and his doctors. You know how that turned out. Mr. Russert's experience is far from unique.

What is so magical about aspirin, Lipitor and a low-fat diet?

There is a simple rationale behind this approach. Aspirin doesn't reduce atherosclerotic plaque growth, but it inhibits the propagation of a blood clot on top of a coronary plaque that has "ruptured," thereby reducing likelihood of heart attack (which occurs when the clot fills the artery). So aspirin only provides benefit if and when a plaque ruptures.

Lipitor and other statin drugs reduce LDL cholesterol, promote a modest relaxation of constricted plaque-filled arteries (normalization of endothelial dysfunction), and exerts other effects, such as inflammation suppression.

A low-fat diet is intended to reduce saturated fat that triggers LDL cholesterol formation and to encourage intake of whole grains that reduce cardiovascular events and LDL cholesterol.

If that is the extent of your heart disease prevention program, you will have a heart attack, bypass surgery, or stent--period. It may not be tomorrow or next Friday, or even next month. Aspirin, Lipitor, and a low-fat diet may delay your heart attack or procedure for a few years, but it will not stop it.

Some flaws in the aspirin, Lipitor, low-fat program:

--Aspirin can only exert so much blood clot-blocking effect. It can be overwhelmed by many other factors, such as increased blood viscosity, increased fibrinogen (a blood clotting protein that also triggers plaque), and plaque inflammation.
--Lipitor reduces LDL, but does not discriminate between the relatively harmless large LDL and the truly plaque-triggering small LDL--it reduces all LDL, but small LDL can still persist, even at extravagant levels since neither aspirin nor Lipitor specifically reduces small LDL, while a low-fat diet increases small LDL.
--Low-fat diet--A diet reduced in fat and loaded with plenty of "healthy whole grains" will trigger increased small LDL (an enormous effect), c-reactive protein, high blood sugar, resistance to insulin, high blood pressure, and an expanding abdomen ("wheat belly").

Aspirin, Lipitor and a low-fat diet do not address:

--Vitamin D deficiency
--Omega-3 fatty acid deficiency and the eicosanoid path to inflammation
--High triglycerides
--Small LDL particles
--Distortions of HDL "architecture"
--Lipoprotein(a)--the worst coronary risk factor nobody's heard of
--Thyroid status

In other words, the simple-minded, though hugely financially successful, conventional model of heart disease prevention is woefully inadequate.

Don't fall for it.

Who is better off?

John takes Crestor, 40 mg per day:

LDL cholesterol 60 mg/dl
HDL cholesterol 60 mg/dl
Triglycerides 60 mg/dl
Total cholesterol 132 mg/dl

Or Sam:

LDL cholesterol 60 mg/dl
HDL cholesterol 60 mg/dl
Triglycerides 60 mg/dl
Total cholesterol 132 mg/dl

who obtained these values through vitamin D normalization (to increase HDL); wheat elimination (to reduce triglycerides and LDL); and omega-3 fatty acids (to reduce triglycerides).

Believe the drug industry (motto: If some statin is good, more statin is better!), then John is clearly better off: He has obtained all the "benefits" of statin drugs. They refer to the "pleiotropic" effects of statin drugs, the presumed benefits that extend outside of cholesterol reduction. The most recent example are the JUPITER data that demonstrated 55% reduction in cardiovascular events in people with increased c-reactive protein (CRP). Media reports now unashamedly gush at the benefits of Crestor to reduce inflammation.

However, on Sam's program, elimination of wheat and vitamin D both exert anti-inflammatory effects on CRP, typically yielding drops of 70-90%--consistently, rapidly, and durably.

So which approach is really better?

In my experience, there is no comparison: Sam is far better off. While John will reduce his cardiovascular risk with a statin drug, he fails to obtain all the other benefits of Sam's broader, more natural program. John will not enjoy the same cancer protection, osteoporosis and arthritis protection, relief from depression and winter "blues," and increased mental and physical performance that Sam will.

If our goal is dramatic correction of cholesterol patterns and reduction of cardiovascular risk, for many, many people statin drugs are simply not necessary.

In the Track Your Plaque program, we aim to stop or reduce your heart scan score.

Recall that, without any preventive efforts, heart scan scores can be expected to increase at the average rate of 30% per year (faster at lower scores, slower at higher scores by a quirk of arithmetic).

I am continually surprised at how often people--that is, people not in the Track Your Plaque program--are often content with what I term "deceleration," or the slowing of plaque growth. In truth, most people are content with deceleration of plaque growth because they simply don't know that plaque continues to grow.

For instance, the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES)), reported in 2005 showed that 650 women participants continued to increase heart scan scores 15% whether they took "high-intensity" statin therapy in the form of Lipitor 80 mg or "low-intensity" statin therapy as pravastatin 40 mg, even though the group taking Lipitor experienced twice the amount of LDL reduction. In other words, heart scan scores continued to increase at the same rate of 15% per year regardless of the intensity of LDL lowering by statin drug.

Another study reported in 2006, Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months: a multicenter, randomized, double-blind trial reported similar results. Of the 471 participants, those taking Lipitor 80 mg per day experienced 27% per year plaque growth (LDL cholesterol 87 mg/dl); those taking 10 mg Lipitor experienced 25% plaque growth (LDL 107 mg/dl). The intensity of statin therapy made no difference on the rate of plaque growth.

In other words, if we are content to sit back and take Lipitor or other statin drug, follow the conventional American Heart Association low-fat, low-cholesterol diet, we will experience somewhere between 15 to 27% annual plaque growth--year after year.

No wonder that conventional advice offered by your friendly neighborhood doctor will avoid (postpone?) only one heart attack in four.

Such is the nature of coronary plaque deceleration: growth is modestly slowed, but is not stopped. Nor is it reversed.

In the Track Your Plaque program, we grade deceleration of plaque growth into three distinct stages out of a total of five. (See Winning Your Personal War with Heart Disease: The Track Your Plaque 5 Stages of Success.)

Why be satisfied with deceleration? Why not aim for a total stop to plaque growth? Why not aim for stage 5 of Track Your Plaque success: reversal?

(For followers of the Heart Scan Blog, below is a re-posting of a recent post. I've moved it up to make it accessible to a number of patients that I asked to look at this post for some conversation about the concept of wheat-free diets.)

TV ads, media conversations, magazine articles, even advice from the American Heart Association and USDA (a la Food Pyramid) all agree: eat more whole grains, get more fiber.

What happens when you follow this advice to add more and more whole grains to your diet? Look around you: People gain weight, they become pre-diabetic and diabetic. Lipids and lipoprotein patterns emerge: increased triglycerides and VLDL, reduced HDL, small LDL. Blood sugar goes up, inflammatory responses are ignited. You feel crumby, cancer risk is increased.

"Official" agencies have urged us to eat more grains, get more fiber and most Americans have complied. We now have a nationwide health disaster that will eventually lead to more people with coronary plaque, more heart disease, more heart attack, more heart procedures.

This is why I've been urging patients to go wheat-free. It has proven an extraordinarily and surprisingly effective strategy for:

1) rapid and profound weight loss
2) raising HDL and reducing triglycerides, VLDL, and small LDL
3) reducing blood sugars, pre-diabetes and diabetes

So here I (re-) post just a sampling of the comments sent by readers of the Heart Scan Blog who have given this idea a try.

Barbara W said:

It's true! We've done it. My husband and I stopped eating all grains and sugar in February. At this point, we really don't miss them any more. It was a huge change, but it's worth the effort. I've lost over 20 pounds (10 to go)and my husband has lost 45 pounds (20 to go). On top of it, our body shapes have changed drastically. It is really amazing. I've got my waist back (and a whole wardrobe of clothes) - I'm thrilled.

I'm also very happy to be eating foods that I always loved like eggs, avocados, and meats - without feeling guilty that they're not good for me.

With the extremely hot weather this week in our area, we thought we'd "treat" ourselves to small ice cream cones. To our surprise, it wasn't that much of a treat. Didn't even taste as good as we'd anticipated. I know I would have been much more satisfied with a snack of smoked salmon with fresh dill, capers, chopped onion and drizzled with lemon juice.

Aside from weight changes, we both feel so much better in general - feel much more alert and move around with much greater flexibility, sleep well, never have any indigestion. We're really enjoying this. It's like feeling younger.

It's not a diet for us. This will be the way we eat from now on. Actually, we think our food has become more interesting and varied since giving up all the "white stuff". I guess we felt compelled to get a little more creative.

Eating out (or at other peoples' places) has probably been the hardest part of this adjustment. But now we're getting pretty comfortable saying what we won't eat. I'm starting to enjoy the reactions it produces.

Weight loss, increased energy, less abdominal bloating, better sleep--I've seen it many times, as well.

Dotslady said:

I was a victim of the '80s lowfat diet craze - doc told me I was obese, gave me the Standard American Diet and said to watch my fat (I'm not a big meat eater, didn't like mayo ... couldn't figure out where my fat was coming from! maybe the fries - I will admit I liked fries). I looked to the USDA food pyramid and to increase my fiber for the constipation I was experiencing. Bread with 3 grams of fiber wasn't good enough; I turned to Kashi cereals for 11 years. My constipation turned to steattorrhea and a celiac disease diagnosis! *No gut pains!* My PCP sent me to the gastroenterologist for a colonscopy because my ferritin was a 5 (20 is low range). Good thing I googled around and asked him to do an endoscopy or I'd be a zombie by now.

My symptoms were depression & anxiety, eczema, GERD, hypothyroidism, mild dizziness, tripping, Alzheimer's-like memory problems, insomnia, heart palpitations, fibromyalgia, worsening eyesight, mild cardiomyopathy, to name a few.

After six months gluten-free, I asked my gastroenterologist about feeling full early ... he said he didn't know what I was talking about! *shrug*

But *I* knew -- it was the gluten/starches! My satiety level has totally changed, and for the first time in my life I feel NORMAL!

Feeling satisfied with less is a prominent effect in my experience, too. You need to eat less, you're driven to snack less, less likely to give in to those evil little bedtime or middle-of-the-night impulses that make you feel ashamed and guilty.

An anonymous (female) commenter said:

My life changed when I cut not only all wheat, but all grains from my diet.

For the first time in my life, I was no longer hungry -no hunger pangs between meals; no overwhelming desire to snack. Now I eat at mealtimes without even thinking about food in between.

I've dropped 70 pounds, effortlessly, come off high blood pressure meds and control my blood sugar without medication.

I don't know whether it was just the elimination of grain, especially wheat, or whether it was a combination of grain elimnation along with a number of other changes, but I do know that mere reduction of grain consumption still left me hungry. It wasn't until I elimnated it that the overwhelming redution in appetite kicked in.

As a former wheat-addicted vegetarian, who thought she was eating healthily according to all the expert advice out there at the time, I can only shake my head at how mistaken I was.

That may be a record for me: 70 lbs!!

Stan said:

It's worth it and you won't look back!

Many things will improve, not just weight reduction: you will think clearer, your reflexes will improve, your breathing rate will go down, your blood pressure will normalize. You will never or rarely have a fever or viral infections like cold or flu. You will become more resistant to cold temperature and you will rarely feel tired, ever!

Ortcloud said:

Whenever I go out to breakfast I look around and I am in shock at what people eat for breakfast. Big stack of pancakes, fruit, fruit juice syrup, just like you said. This is not breakfast, this is dessert ! It has the same sugar and nutrition as a birthday cake, would anyone think cake is ok for breakfast ? No, but that is exactly the equivalent of what they are eating. Somehow we have been duped to think this is ok. For me, I typically eat an omelette when I go out, low carb and no sugar. I dont eat wheat but invariably it comes with the meal and I try to tell the waitress no thanks, they are stunned. They try to push some other type of wheat or sugar product on me instead, finally I have to tell them I dont eat wheat and they are doubly stunned. They cant comprehend it. We have a long way to go in terms of re-education.

Yes. Don't be surprised at the incomprehension, the rolled eyes, even the anger that can sometimes result. Imagine that told you that the food you've come to rely on and love is killing you!

Anne said:

I was overweight by only about 15lbs and I was having pitting edema in my legs and shortness of breath. My cardiologist and I were discussing the possible need of an angiogram. I was three years out from heart bypass surgery.

Before we could schedule the procedure, I tested positive for gluten sensitivity through www.enterolab.com. I eliminated not only wheat but also barley and rye and oats(very contaminated with wheat) from my diet. Within a few weeks my edema was gone, my energy was up and I was no longer short of breath. I lost about 10 lbs. The main reason I gave up gluten was to see if I could stop the progression of my peripheral neuropathy. Getting off wheat and other gluten grains has given me back my life. I have been gluten free for 4 years and feel younger than I have in many years.

There are many gluten free processed foods, but I have found I feel my best when I stick with whole foods.

Ann has a different reason (gluten enteropathy, or celiac disease) for wanting to be wheat-free. But I've seen similar improvements that go beyond just relief of the symptoms attributable to the inflammatory intestinal effects of gluten elimination.

Wccaguy said:

I have relatively successfully cut carbs and grains from my diet thus far.

Because I've got some weight to lose, I have tried to keep the carb count low and I've lost 15 pounds since then.

I have also been very surprised at the significant reduction in my appetite. I've read about the experience of others with regard to appetite reduction and couldn't really imagine that it could happen for me too. But it has.

A few weeks ago, I attended a party catered by one of my favorite italian restaurants and got myself offtrack for two days. Then it took me a couple of days to get back on track because my appetite returned.

Check out Jimmy Moore's website for lots of ideas about variations of foods to try. The latest thing I picked up from Jimmy is the good old-fashioned hard boiled egg. Two or three eggs with some spicy hot sauce for breakfast and a handful of almonds mid-morning plus a couple glasses of water and I'm good for the morning no problem.

I find myself thinking about lunch not because I'm really hungry but out of habit.

The cool thing too now is that the more I do this, the more I'm just not tempted much to do anything but this diet.

Going wheat-free, along with a reduction in processed sugary foods like Hawaiian Punch, sodas, and candy, is the straightest, most direct path I know of to lose weight, obtain all the health benefits listed by our commenters, as well as achieve the lipoprotein corrections we seek, like reduction of small LDL particles and rise in HDL, in the Track Your Plaque program.

Followers of the Track Your Plaque program know that we advocate periodic fasts to reduce heart disease risk.

I came across an interesting report form an abstract presented at last week's American Heart Association meetings in Orlando:

(Read the report at HeartWire. You will need to register or sign-in.)

In this study, the investigators tried to determine why members of the Church of Jesus Christ of Latter-Day Saints (LDS) tended to have reduced risk of heart disease compared to others in the area but not in the LDS faith. While the reduced risk of heart disease in LDS members had been traditionally attributed to the no smoking policy advocated by the Mormon church, the investigators suspected that there was more to the reduced risk.

Of 515 people interviewed, periodic fasting, whether for religious or other reasons, was found to distinguish people who were less likely to have coronary disease by conventional catheterization (59% vs. 67%). (Since the study was published in only abstract form, it's not clear why all these people underwent heart catheterization in the first place.)

Nonetheless, it's an interesting observation and one consistent with the benefits we see when someone fasts: reduced blood pressure, reduced inflammatory responses, improved lipids and lipoproteins, weight loss.

Fasting can be an especially effective method to gain control over heart disease and coronary plaque if rapid control is desired. In fact, I wonder if the normally year-long process of plaque control that I advocate can be much abbreviated. Fasting, I believe, is a crucial component of rapid control, what I've talked about in Instant Heart Disease Reversal

There's also additional thoughts on fasting in my Heart Scan Blog post, For rapid success, try the "fast" track.

Fasting is not something to fear. It can be an enlightening process that can serve to abruptly sever bad habits, perhaps even turn the clock back on prior dietary and lifestyle excesses. My favorite variation on fasting is to use soy milk (yes, yes, I know! I can already hear the the soy bashers screaming!) as a meal substitute. It is an easy, less dramatic way that still maintains most of the benefit of a full, water-only fast.

Why do stress tests so often fail to detect coronary atherosclerotic plaque? Why do even heart catheterizations--the "gold standard"--fail to disclose the full extent of plaque within the walls of coronary arteries?

We owe much of the explanation of these phenomena to Dr. Seymour Glagov, retired professor of pathology at the University of Chicago.

When studying the coronary arteries of people who died, he observed that people commonly had plenty of atherosclerotic plaque lining the artery wall, yet it did not necessarily impinge on the artery "lumen," or the internal path for blood to flow.

The only time the lumen became obstructed by plaque was when either 1) plaque grew to overwhelming levels and was severe and extensive, or 2) when a plaque had "ruptured," meaning its thin covering had been penetrated and eroded by the underlying plaque tissue like a volcano emerging from the surface and erupting.

This groundbreaking observation, now dubbed "the Glagov phenomenon," explains why someone can have a normal stress test on Tuesday but erupt a plaque on Wednesday.

The Glagov phenomenon also explains why heart scans can detect plaque when both stress tests and heart catheterizations fail to do so. Many physicians will then interpret this to mean that the heart scan was wrong. With the Glagov phenomenon in mind, you can see that the heart scan is not wrong, it is simply detecting coronary atherosclerotic plaque at a stage that is not yet detectable by the other methods.

In the illustration, you can see that the lumen of the vessel is maintained--despite the artery on the left having minimal plaque, the artery on the right containing moderate plaque. If either artery were examined by a test that relies on blood flow--stress test or heart catheterization--both would appear normal. But a test that examines the artery wall, such as a heart scan, would readily detect the artery on the right and probably even the artery on the left.

I am very grateful to Dr. Glagov and his insight into this important process. Otherwise, we might still be floundering around trying to understand the apparent discrepances between these tests that simply provide different perspectives on the same problem.

I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

Of course, the medical literature is swamped with studies that have nothing to do with reversal, like what stent is best, what platelet-inhibiting intravenous drug is best, when should angioplasty or stents be used and when, do implantable defibrillators save lives, improvements in coronary bypass techniques, etc. There are tens of thousands of these studies for every study that focuses on the question of atherosclerotic plaque reversal.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease ? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.

Once upon a time, remember how medical information was mysterious, hospitals were places where frightening, inscrutable things happened, diseases were strange maladies that struck without reason, and obtaining information about health was like hunting for buried treasure? The full extent of many peoples' understanding of health came through relatively anemic sources like Readers' Digest. (Remember "I am Joe's Colon"?)

Compare this to what we have now. If I wanted to obtain information about ankylosing spondylitis (a rare genetic disease of the spine), a Google search yields 1.46 million citations. Not all the information, of course, is helpful or relevant, but there's certain to be a bounty of information that far exceeds what you could have uncovered 40 years ago.

Suppose you enter the search phrase "antithrombin III" into your Google search. Citations: over 900,000. (The number of search citations, in fact, exceeds the number of Americans with a deficiency of this blood clotting protein!)

The same is true with heart disease. There was a time, not more than 30-40 years ago, when information about the heart and heart disease was hard to come by. The most you would find were superficial discussions about heart attacks, what chest pain means, descriptions of bypass surgery. Ask your doctor, you'd likely receive a brief, cursory response about how you probably shouldn't worry it.

Even during medical school in the 1980s, I remember struggling to get answers to my questions from faculty during medical school and medical training. It was as if providing too much information would eliminate the advantage superiors wielded over trainees.

The same selfish sentiment, the "I know something you don't know" mentality reminiscent of a schoolboy's "naa na na naa naa!" unfortunately persists. But it is rapidly disintegrating. Soon it will join the junk heap of medical mis-information accumulated over the years (a big pile, to be sure). The internet and, I'll admit (grudgingly), the media, have been responsible for demystifying the formerly mysterious and indecipherable world of health.

You now have, at a moment's disposal, access to an extraordinary array and breadth of health information that was inconceivable just a few years ago.

Times are changing. Doctors no longer hold the monopoly over health information. The public--YOU--are rapidly becoming the arbiters of health, the informed consumers of a soon-to-be retail product called health care, and the increasingly savvy judges of what should join the mainstream path of health. It is all part of this wave of change that I've been advocating: the emerging concept of self-empowerment in healthcare.

Added to the junk heap of health-mistakes-of-years-past will be medical protectionism over health information, heart procedures, drug industry excesses, nutritional mis-information, among others. The demystification of health information will open the floodgates of individual insight into health. It delivers control over your own health destiny straight into your own lap.

Walking the supermarket aisles, you may have lately noticed that numerous new products are appearing sporting "omega-3s" on the label.

Some products simply contain alpha-linolenic acid, a tiny amount of which is converted to the biologically active omega-3s, EPA and DHA. Natural Ovens' Brainy Bagel, for instance, carries a claim of "620 omega-3."

I find this confusing and misleading, since people will often interpret such a claim to mean that it contains 620 of EPA and DHA, similar to two capsules of standard fish oil (1000 mg capsules). Of course, it does NOT. I find this especially troublesome when people will actually stop or reduce their fish oil, since they've been misled into thinking that products like this bread contain active omega-3 fatty acids that yield all the benefits of the "real stuff."

Other products actually contain the omega-3, DHA, though usually in small quantities. Breyer's Smart with DHA is an example, with 32 mg DHA per container.

I find products with actual DHA (from algae) a more credible claim. However, the Center for Science in the Public Interest (CSPI) has looked at the actual contents of DHA in some of these products and found some discrepancies, including amounts of DHA less than the labeled amount and claims of omega-3 wihtout specifying DHA vs. linolenic acid. (It's probably linolenic acid, if it's not specified.)

All in all, the addition of DHA to food products is a nice way to boost your intake of this healthy omega-3. However, keep in mind that these are processed, often highly processed, foods and you will likely pay a premium for the little boost. For now, stick to fish oil, the real thing.

For a brief summary of the CSPI report and a link to the Nutrition Action Newsletter, see Omega-3 Madness: Fish Oil or Snake Oil.

I'm sitting at dinner with two colleagues. One is a cardiology colleague, another an internist who, in addition to practicing general internal medicine, also takes heart disease prevention very seriously. He has, in fact, participated in the Track Your Plaque program and dropped his heart scan score substantially.

"Why don't we see you in the cath lab much?" my cardiology colleague asked me. He was puzzled, since he knew my background in cath lab work from years before, spending day and night doing procedure after procedure. He spends virtually all his days there.

"Well, my patients simply don't have events any more. Heart attacks and angina among people in my program are just about non-existent. They don't have symptoms and they don't have to go to the hospital. I can't remember the last time that I was woken up in the middle of the night for an urgent procedure for one of my patients."

The internist across the table smiled and expressed his agreement. "That's the same thing I'm seeing: No heart attacks, very few if any referrals to cardiologists for procedures. I remember when it was a several times a week thing. Now, almost never. "

Looking at my cardiology colleague, I saw the usual cardiologist reaction: Eyes searching left and right and behind us for something more interesting. Certainly, talking about a virtual cure for coronary heart disease was just too damn dull.

Such is the attitude of 98% of my colleagues: If it doesn't generate a revenue-producing procedure, why bother? Prevention is for general practitioners, the line of thinking goes. "And anyway, I'm too busy doing procedures! I don't ahve time to talk about prevention and health!" Of course, the poor general practitioner is already overloaded with caring for arthritis, flu, diabetes and all the new drugs for diabetes, headaches, vaccinations, diarrhea, and . . .oh, yes, heart disease prevention.

Are cardiologists the enemy? No, of course they are are not. But they often act like they are. Talking to cardiologists is like going to the car dealer with your checkbook out, pen in hand. The salesman gets to write the check himself and you just sign it. Talk to a cardiologist and more often than not you will end up with a heart procedure--whether or not you need it.

Unfortunately--tragically--they often forget what they are supposed to be doing: Taking care of a disease by preventing it. Putting in a defibrillator is not preventing a disease. Putting in three stents, laser angioplasty, and thrombectomy are not ways of preventing a disease.

I'm thankful for my internist friend who sees the light. Coronary heart disease is a an easily measurable, quantifiable, preventable, and REVERSIBLE process for many, if not most, people when provided the right tools. But don't ask your neighborhood cardiologists to give you those tools.

Was torcetrapib’s crash and burn fatal for this class of drug?

At the 2007 American Heart Association meetings in Orlando, Florida, Dr. Philip Barter of Sydney, Australia, presented an update of the ILLUMINATE drug trial for the once-promising drug, torcetrapib, the billion-dollar bet that Pfizer made on its first entry into the new drug class.

You may recall that the crash and burn of Pfizer’s torcetrapib in December 2006 made headlines and prompted enormous disappointment for many patients and doctors who had hoped for a new drug choice to raise HDL cholesterol. Pfizer executives (heads flew!) and investors were also disappointed, anticipating release of a drug that might have become the number one biggest selling drug in the world—ever, surpassing even Lipitor's® $13 billion annual sales.

Torcetrapib is the first among the “cholesteryl-ester transfer protein inhibitors,” or CETP-inhibitors, drugs that block the exchange of cholesterol and triglycerides between HDL and VLDL particles and prevent formation of the unwanted small LDL particles. Preliminary efforts suggested that effects were positively enormous.

However, the 15,000-participant trial was abruptly terminated after 550 days when an excess of deaths were identified among the group taking the experimental drug: 59 deaths in control group; 93 deaths in the torcetrapib group.

In addition, cardiovascular events were 24% greater in the torcetrapib group, numbering 373 compared to 464 in the no-torcetrapib group, including a substantially greater number of heart attacks and hospitalizations. Another surprise came in the way of cause of death among some of the torcetrapib patients, with an excess of deaths due to cancers (twice as many in the torcetrapib group), strokes, and infections.

Why the divergence: enormous improvements in cholesterol values, yet increase in adverse effects including more heart attack? Deeper digging by the principal investigators uncovered unexpected distortions of electrolytes like sodium and potassium. They then re-analyzed blood samples from participants on both sides of the trial and discovered that participants taking torcetrapib experienced significant rise in the blood pressure hormone, aldosterone. This, they surmised, also likely accounted for the 4 mmHg average rise in blood pressure among those taking the experimental drug. (This is the same pathway blocked by blood pressure drugs like ACE inhibitors lisinopril and enalapril, ARBs like losartan.)

Simultaneously (what a coincidence!) with the torcetrapib data, investigators at competing drug manufacturer, Merck, reported encouraging data with their version of CETP inhibitor, anacetrapib. In a phase II FDA trial of 589 patients, anacetrapib reduced LDL-C levels by up to 40% and increased HDL-C up to 139%.

Spokesman Daniel Bloomfield, M.D., of Merck Research Laboratories reported that "The favorable lipid effects seen in this study with multiple doses of anacetrapib were significant, and confirm the continued evaluation of the clinical benefits of CETP inhibitors in the treatment of dyslipidemia." Quick to distinguish this drug from torcetrapib’s track record of dangerous effects on blood pressure, he added that "the decreased LDL-C concentrations, increased HDL-C concentrations and no demonstrable increase in blood pressure seen with anacetrapib are particularly encouraging results of this study."

However, the data reported only an 8 week expereince. Given the experience with torcetrapib, longer term data will obviously be required to assess safety. After Pfizer spent over $1 billion and sacrificed lives to obtain this experience, Merck will need to tread carefully.

It will clearly be many years before we have a confident answer on whether the CETP-inhibitor class of drugs will be a safe choice for correction of cholesterol abnormalities, especially low HDL. Are we helpless until then?

Though CETP inhibitors offer the potential for a one-stop opportunity to raise HDL substantially, there are still many strategies available to raise HDL.

Strategies that raise HDL and are available today include:
• Weight loss—to your ideal weight. A very effective strategy.
• Reduction in processed carbohydrates—like breads, pasta, cookies, pretzels, etc. Note that very low-fat diets reduce HDL. Often a huge effect.
• Fish oil—A small effect, more dramatic when triglycerides are high.
• Niacin—Vitamin B3, the best we have at present. Doses of 500-1500 mg per day raise HDL 20–50%; work with your doctor if you are contemplating niacin. We use this agent everyday and have had great success; good hydration is key to minimize the annoying “hot-flush” effect.
• Dark chocolate—40 grams, or about 2 inches square, a delicious way to squeeze out a little rise in HDL.
• Alcoholic beverages—Red wines are almost certainly the preferred route, rich in flavonoids.
• Exercise—HDL-raising effects vary, but can sometimes be as much as 10–20 mg.
• Other drugs—Though not commonly used for this effect, drugs like pioglitazone (for diabetes and pre-diabetes); fibrates (Tricor® or fenofibrate; Lopid® or gemfibrozil); and Pletal® or cilostazol are occasionally prescribed.
• Vitamin D—You won’t find validation of this effect in any scientific study, but our emerging experience in our heart disease reversal program is suggesting that this neglected nutrient can exert powerful HDL-raising effects. In fact, supplementing vitamin D has made my life much easier.

And, last I checked, none of these HDL-raising strategies are ever fatal.

Joe, a machinist, was frightened and frustrated.

With a heart scan score of 1644 at age 61, his eyes bulged when I advised him that, if preventive efforts weren't instituted right away, his risk for heart attack was a high as 25% per year. Joe had "passed" a stress test, thus suggesting that, while coronary plaque was present--oodles of it, in fact--coronary blood flow was normal. Thus, there would be no benefit to inserting three stents, say, or a bypass operation.

(Illustration courtesy Wikipedia)

"I don't get it, doc. Why can't you just take it out? You know, like Roto-Rooter it out? Or give me something to dissolve it!"

Of course, if there were such a thing, I'd give it to him. But, of course, there is not. It doesn't mean that there haven't been efforts in this direction over the years. Among the various attempts made to "Roto-Rooter" atherosclerotic plaque have included:

Coronary endarterectomy
This is a drastic procedure rarely performed anymore but enjoyed some popularity in the 1980s and 1990s. Coronary endarterectomy was performed during coronary bypass surgery, but few thoracic surgeons performed it. Milwaukee's Dr. Dudley Johnson was the foremost practitioner of this procedure (retired a few years ago after his own bypass operation) with a mortality in excess of 25%. A very dangerous procedure, indeed. The technical hurdle, beyond the tedium and length of time required to remove plaque that had a tendency to fragment, was blood clot formation after tissue was exposed upon plaque removal. I saw many lengthy hospital stays and deaths following this procedure.

Coronary atherectomy
This is an angioplasty-type procedure that has gone through several variations over the years.

In the early 1990s, transluminal extraction atherectomy (TEC) was a technique involving low-rpm drill bits with a suction apparatus that was used to clear soft debris, usually from large coronary arteries or, more commonly, bypass grafts. Then came direction atherectomy, in which a steel housing contained a sharp drill bit that captured atherosclerotic plaque in an aperture along the housing length and stuffed it into a nosecone, retrieved once the device was removed.

Then came high-speed rotational atherectomy in which a diamond-tipped drill bit rotated up to 200,000 rpm and essentially pulverized plaque to flow downstream and, presumably, eventually captured by the liver for disposal. Rotational atherectomy is still in use on occasion. Laser angioplasty, usually using the excimer wavelength, vaporizes plaque. I did plenty of all of these back in the early and mid-1990s.

While all atherectomy procedures sound clever, they are all plagued by the same problem: vigorous return of plaque. Remove plaque, it grows back. There are few instances today in which atherectomy is still performed.

Chelation
This involves a metal-binding, or "chelating," agent like EDTA normally used in conventional practice for lead poisoning. Usually administered IV, some have also advocated oral use. People who use chelation also tend to believe in faith healing and other practices based on faith, not science. There is an international trial that is nearing completion that should provide the final word on whether there is any role to intravenous chelation.

There are numerous other oral treatments that claim a Roto-Rooter-like effect. Nattokinase, for example--an outright, unadulterated, and unqualified scam.

Unfortunately, the helpless, ignorant, and gullible are many. When frightened by the specter of heart disease, there are plenty of people who will willingly pay for the hope provided by clever ads, fast-talking salespeople, and unscrupulous practitioners.

So, Joe, there is no Roto-Rooter for coronary atherosclerotic plaque, at least one that is safe, doesn't involve a life-threatening effort, provides results that endure beyond a few months, and truly works.

The Track Your Plaque program may not be easy. There are obvious common hurdles to adhering to these concepts: obtaining lipoprotein testing, getting intelligent interepretation of the results, persuading your doctor to measure vitamin D blood levels, battling the onslaught of prevailing food propaganda that confuses and misleads. The Track Your Plaque program also requires time, at least a year.

But it's the best program there is. Do you know of anything better?

It is the craziest thing.

The notion of vitamin D being easily and readily toxic has grabbed hold of many people, including my colleagues who were taught that vitamin D was toxic in medical school based on the skimpiest (and often misinterpreted) observations in a handful of unusual cases.

In my practice and in the Track Your Plaque program, we routinely use doses of 2000-10,000 units per day, occasionally more. We are guided by blood levels of 25(OH) vitamin D3. I have personally never witnessed vitamin D toxicity.

Here's an interesting graph from Dr. Reinhold Vieth. Those of you familiar with the vitamin D argument know that Dr. Vieth is among the few genuine gurus in the vitamin D world.

From Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr 1999;69:842-856. (Full text is available without charge.)

In the graph, the X's represent toxicity; circles fall within the non-toxic range. (Toxicity is generally defined as a level sufficient to raise blood calcium levels, "hypercalcemia.") Note that the 25(OH) vitamin D3 levels are given in nmol/L; to convert to ng/ml units that are customary in the U.S., divide the nmol/L value by a factor of 2.5.

You will notice that toxicity is virtually unheard of until the dose exceeds 10,000 units per day. Beyond 10,000 units per day, the curve heads upward sharply and toxicity does become a possibility, though not an absolute (since there are circles above 10,000 units).

You may also notice that the curve is relatively flat from vitamin D doses between 200 units and 10,000 units (log scale on x axis; arithmetic scale on y), the range of most common doses for vitamin D supplementation.

Another perspective on vitamin D blood levels is to examine the blood levels of people who are young and obtain plentiful sun exposure. Lifeguards, for instance, have blood levels of 84 ng/ml (210 nmol/L) without ill-effect. (Sun exposure cannot generate vitamin D toxicity, because of a feedback safety mechanism in skin.) While this may not represent an ideal level since they represent an extreme, it does provide reassurance that such levels are non-toxic. I also point out these levels occur in the youthful since most people lose 75% or more of vitamin D activating capacity in the skin by their 70s. Most of us over 40 are kidding ourselves if we think that a suntan provides sufficient vitamin D.

Keep in mind that it is not necessarily the dose of vitamin D that is toxic, but the blood level it generates. I take 10,000 units of vitamin D as a gelcap per day to maintain my blood level between 50-60 ng/ml (125-150 nmol/L). This strategy helps me keep my HDL in the 70-80 mg/dl range, my blood sugar around 90 mg/dl, my blood pressure <120/80, and I no longer experience colds nor winter "blues."

Copyright 2008 William Davis, MD

For reasons unknown to me, I received a solicitation to invest in a company called Prescient Medical, with a slogan that caught my eye:

Detect and treat heart attacks before they occur.

The glossy brochure details their technology development strategy:

Predict(TM) Optical Catheter System--A catheter introduced into the coronary artery during a catheterization procedure to determine whether a specific plaque or vessel area is "vulnerable," i.e., prone to rupture in future.

Protect(TM) Luminal Shield--A stent-like metal device deployed into the coronary artery at the region of vulnerable plaque to prevent future plaque rupture.

The company anticipates FDA approval for their systems by 2009 and sales to begin by 2010. They predict sales of $7 billion.

Let's stop and think about this for a moment. It seems to me that, rather than pursuing the market of another stent for a "severe blockage," this company is going after the untapped procedural market of vulnerable plaque. In other words, their technology (an optical sensor technology that emits and analyzes light wavelengths to map specific plaque characteristics) identifies plaque that may rupture in months or years, followed by implantation of stent(s) that presumably prevent plaque rupture.

Thus, conceivably, many 20%, 30%, 40% etc. "blockages", atherosclerotic plaques that do not block flow and thereby pose no need for a conventional stent, will end up with this new type of stent. One patient could therefore receive multiple "Luminal Shields" in a single procedure.

When would these devices be employed? One pathway I could conceive of that my colleagues will be sure to exploit is 1) identify plaque by CT angiography, then 2) bring patient to the catheterization laboratory and perform this procedure for whatever hot, vulnerable plaques are identified. In other words, symptoms are no longer necessary. Reduced blood flow is no longer necessary. An abnormal stress test is no longer necessary. All that is required is that you have plaque. If the plaque is then determined to be vulnerable, then it is stented.

What bothers me about all this is the emerging effort to exploit this untapped market--a big one--of early heart disease as identified by coronary atherosclerotic plaque. As heart scans have demonstrated, there is an enormous amount of hidden heart disease in this world. This company has discovered a way to turn plaque into a profit opportunity, much as the statin drug industry found a way to "turn cholesterol into money."

The conventional stent market has plateaued and now has been, to some degree, battered by the drug-coated stent argument. Prescient has found a new and significant market for procedures and stents.

Is this really necessary? Why does plaque have to become a procedural disease? Doesn't it make more sense that, if vulnerable plaque is identified, that clinical trials are then designed to develop treatment strategies that modify vulnerable characteristics? Shockingly, this has not been done to any significant extent. Instead, the easiest path to a profit opportunity is to implant a "Luminal Shield."

You and I are able to inactivate, disempower, and essentially shut down plaque, while others are working furiously to convert it into a procedural profit opportunity. I personally find this so distasteful that I would sooner endorse a high-dose statin strategy than this approach.

You can view a video of my colleague, Dr. Martin Leon, on the Prescient Medical website, (or click here to go directly to the video), talking about how this technology will "change the treatment paradigm of the interventionalist from reactive to proactive." Scary stuff. Dr. Leon has made millions of dollars (probably more like tens of millions of dollars) from his support of technology companies for the interventional coronary device market.

My hope is that word of the sorts of techniques we use in the Track Your Plaque program disseminate before this sort of luminal coating idiocy gets off the ground.

(In actuality, a different version of this approach has been available for years using intravascular ultrasound (IVUS), another procedure that involves threading a catheter down each coronary artery during a catheterization procedure. IVUS can also cross-sectionally map a plaque's anatomy and identify "vulnerable" features, like a thin cap overlying a collection of semi-liquid fat ("lipid pool"). There has been some discussion of using this approach to identify vulnerable plaque followed by stent implantation, but it has never gotten off the ground and has certainly not found validation in any clinical study. By the way, any stent prevents plaque rupture, since by their very nature, the plaque contents are compressed, modified, and excluded to the exterior of the stent. Plaque rupture within a stent is very rare in its few millimeters of length. It may therefore not require some new technology to prevent plaque rupture.)

Evan's first heart scan score in November, 2006 yielded a high score for a 56-year old male: 542.

So he put up little fuss when his doctor prescribed simvastatin at a high dose.

Evan's LDL cholesterol before simvastatin: 158 mg/dl

Evan's LDL cholesterol on simvastatin: 72 mg/dl.

By conventional standards, Evan has had an excellent response. The rest of his lipid (cholesterol) panel was unrevealing: HDL 62 mg/dl, triglycerides 78 mg/dl. Evan doesn't smoke, has a normal blood pressure, and he is not diabetic. That should do it, right?

So his doctor thought. So Evan asked if another heart scan was in order. In December, 2007, after one year of simvastatin, his second heart scan score: 705--a 30% increase over one year.

Recall that, with no effort at prevention whatsoever, the natural progression of heart scan scores is a 30% per year increase. Did simvastatin do nothing?

This is quite typical of people who do nothing more than take a statin drug. While some people do slow plaque growth (we say "decelerate") modestly on a statin drug, Evan's experience is not unusual: plaque continues to grow despite high-dose statin drug and an apparently favorable cholesterol panel.

In fact, I can count the number of people who reduced their heart scan scores taking a statin drug alone on one finger.

Statins do not represent a cure for heart disease. They cannot be used as sole therapy to reduce risk for heart attack. In fact, given sufficient time, the majority of people who do nothing more than follow this standard line of treatment (along with the equally lame low-fat diet, etc.) will have done nothing more than postpone their heart attack. Elimination of risk? Nope.

This is among the reasons we developed the Track Your Plaque approach. While not foolproof, I know of no better approach to seize control over plaque growth.

Additional conversations on clinical studies which, as with Evan's experience, demonstrated how statin drugs fail to slow plaque growth can be found in previous Heart Scan Blog posts:

Don't be satisfied with "deceleration"

Study review: Yet another Lipitor study

Copyright 2008 William Davis, MD

Triglycerides are a potent trigger for coronary plaque growth.

Triglycerides in and of themselves probably do not cause plaque growth. Instead, triglycerides contribute to the formation of abnormal lipoproteins in the blood that, in turn, trigger coronary plaque, like VLDL, intermediate-density lipoprotein (IDL), and small LDL. Excess triglycerides also modify HDL structure and cause you to lose HDL in the urine.

I see plenty of people who begin with triglycerides of 200 mg/dl, 300, 700, even over 1000 mg/dl. It doesn't take long before you learn what works, what doesn't to reduce triglycerides. This is especially true in the Track Your Plaque approach, in which our target for triglycerides is 60 mg/dl or less.

Here's a list of things to consider if you are trying to gain control of your triglycerides:

--Fish oil--A mainstay of treatment. The omega-3 fatty acids from fish oil are the number one most potent treatment for high triglycerides.

--Reduction of high-glycemic index foods--Most notably wheat. Everybody knows that we shouldn't eat Snickers bars or bags of licorice. But many people eat plenty of wheat-containing breads, pastas, pretzels, crackers, breakfast cereals, etc., all in the name of increasing whole grains and fiber. In reality, they are causing triglycerides to skyrocket, dropping HDL, forming small LDL, increaaing blood sugar and blood pressure, and increasing obesity.

--Eliminating fructose and high-fructose corn syrup--This ubiquitous sweetener is now consumed in enormous quantities by the average American, nearly 80 lbs per year per person. You'll find it in soft drinks, ketchup, beer, breads, breakfast cereals, and many other processed foods. You'll find none in green peppers, cucumbers, and raw nuts. Fructose causes large rises in triglycerides, as well as diabetic patterns. Don't let "fat-free" claims fool you. Take a look at the ingredients in Kraft Fat-Free Caesar Italian salad dressing, for instance:

Kraft Fat-Free Caesar Italian

Ingredients:
Water, Vinegar, High Fructose Corn Syrup, Corn Syrup, Salt, Parmesan Cheese, Part-Skim Milk, Cheese Culture, Salt, Enzymes, Contains less than 2% of Garlic, Whey, Onion Juice, Autolyzed Yeast Extract, Phosphoric Acid, Worcestershire Sauce, Vinegar, Molasses, Corn Syrup, Water, Salt, Caramel Color, Dried Garlic, Sugar ,Spices, Tamarind, Natural Flavors, Hydrolyzed Soy Protein, Xanthan Gum, Potassium Sorbate and Calcium Disodium EDTA as Preservatives, Dried Garlic, Buttermilk, Spice, Dried Parsley, Caramel Color, Sodium Phosphate, Oleoresin Paprika.

--Alcohol--While a couple of drinks a day raises HDL, exerts anti-inflammatory effects, and reduces blood pressure, more than this begins to raise triglycerides. Although I've come across no formal studies on this question, my gut sense is that beer, in particular, raises triglycerides more than wine or other alcoholic beverages. Could it be the wheat source of beer? Or its high-fructose corn syrup? I don't know, but beer is the least desirable form of alcohol of the choices we have.

Following these simple steps, it is unusual in my experience that you cannot achieve a triglyceride level <60 mg/dl. Rarely do we need to add fibrate drugs or other prescription agents to reduce triglycerides.

Copyright 2008 William Davis, MD

Lipoprotein(a), or Lp(a), is a problem area in coronary plaque reversal.

While our current Track Your Plaque record holder for largest percentage reduction in heart scan score has Lp(a), it remains among the more troublesome lipoprotein patterns.

One unique treatment for Lp(a) is high-dose omega-3 fatty acids from fish oil. While the data are relatively meager, there is one solid study from Lp(a) expert, Dr. Santica Marcovina of the University of Washington, called "The Lugalawa Study."

In this unique set of observations, 1300 members of a Bantu tribe living in Tanzania were studied. What made this population unusual is the fact that two groups of Bantus lived under different circumstances. One group lived on Nyasa Lake (3rd largest lake in Africa and reputed to have the greatest number of species of fish of any lake in the world) and ate large quantities of freshwater fish providing up to 500 mg of omega-3s, EPA and DHA, per day. Another Bantu group lived away from the lake as farmers, eating a pure vegetarian diet without fish.

Nyasa Lake

This situation among genetically similar stock provided a unique learning opportunity, a chance to assess whether different diets influenced Lp(a) levels.

The results: The fish-eating Bantus had an average Lp(a) level of 14.0 mg/dl. The farming, non-fish eating Bantus had an average Lp(a) of 27.0--a 48% difference. Curiously, a comparison of the apo(a) component of Lp(a) between the groups also showed that the fisherman expressed fewer dangerous small apo(a) forms, despite equal potential to express both.

The Lugalawa Study opens the question of whether similar results can be obtained not by moving to Tanzania and fishing Nyasa Lake, but by mimicking their experience by supplementing high doses of omega-3 fatty acids.

It's an intriguing question. In the Track Your Plaque program, we have no specific experience with this strategy, but it is certainly worth exploring further.

Watch for two upcoming Special Reports on the Track Your Plaque website in which we will be detailing 1)unique strategies for Lp(a) reduction, and 2) the usefulness of high-dose fish oil for coronary plaque reversal.

Interesting enough for a Virtual Clinical Trial?

Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

Pam has an LDL cholesterol of 144 mg/dl.

To most people, this means that she has a mildly elevated LDL value. Many people would respond by cutting the saturated fat in their diet. Most physicians would concur and talk about prescribing a statin drug.

Let me tell you what an LDL cholesterol of 144 mg/dl means to me:

1) It could mean an LDL of all large particles (which is good) or an LDL of all small particles (which is very bad). Or, perhaps it's some combination of big and small. I can't tell which just by knowing that LDL is 144.

Small LDL responds to a diet reduced in processed carbohydrates and wheat flour; large LDL does not. Small LDL responds in an exagerrated way to niacin; large LDL does not. It makes a difference.

2) It could mean that, hidden within LDL, is lipoprotein(a), or Lp(a). Recall that Lp(a) is a high-risk genetic pattern that can provide the false appearance of high LDL cholesterol. If Pam were prescribed a statin drug, it would have little effect and little benefit. (See Red flags for Lipoprotein(a).)

Knowing that Pam has Lp(a) can point us in an entirely different direction than just LDL cholesterol. It might mean high-dose fish oil, a more serious approach to niacin, hormonal treatments like DHEA or testosterone. It might mean more attention to warning your children about the possibility that they, too, might share this genetic trait.

3) It could mean both small LDL and Lp(a) are present simultaneously, an especially dangerous combined pattern that is among the highest risks for heart disease known.

4) Because Pam's LDL of 144 mg/dl was not measured, but calculated, it means that it is subject to tremendous inaccuracy.

In my office, calculated LDL cholesterols can be inaccurate by 50 or 100 mg/dl--commonly. So Pam's LDL of 144 mg/dl could really be 70 mg/dl, or it could be 244 mg/dl. Once again, it's a big difference.

Just like The Three Faces of Eve, the 1957 film in which Joanne Woodward played the three wildly different sides of Eve's personality--the daytime Eve White, the fun-loving and daring Eve Black, and Jane--so can LDL assume several different faces, all with different personalities, different implications.

Accepting LDL cholesterol as LDL cholesterol is a fool's game. It is only a starting point, nothing more. Accepting a statin drug based on LDL is, likewise, a trap fraught with uncertainty, the potential for limited or ineffective results, the price being your heart and health.

Don had an angioplasty 6 months ago. When asked about the symptoms that prompted him to go to the hospital, he explained:

"I remember feeling really tired for about a week before I went. I'd read that fatigue can sometimes be a sign of heart disease. But then I had some trouble breathing. You know, like not being able to get a deep breath."

"My wife and I were planning on going on vacation. So I wanted to be certain something wasn't going on in my heart. That's when my wife insisted that she take me to the hospital.

"I kind of remember going there and arriving in the emergency room, but then I don't remember anything. Next thing I know, I'm waking up in a hospital bed. My wife and kids were there, looking all concerned. They said that I just got two stents and that the doctor just barely saved my life."

Happy story, happy ending? Not quite.

I reviewed the angiograms made during Don's hospital stay. They did, indeed, show some plaque, but not anywhere close to the amount necessary to account for symptoms like fatigue or breathlessness. For symptoms like this to occur without physical exertion, say, at your desk or relaxing at home, a critical >90% blockage would be required.

The worst "blockage" Don had was 50% at most. The leap was made to connect his relatively vague symptoms with these "blockages," leading to the implantation of two stents.

This is not as uncommon as you think. Yes, the practice of cardiology can be a life of acute procedures, urgent situations, and crises. Unfortunately, some people with questionable need for these procedures also get swept up in the wave. Sometimes it's due simply to the doctor's need to do "something," nervous family waiting in the wings. Sometiems it's intellectual laziness: putting in two stents seems to satisfy many patients' needs to have something "fixed," even when symptoms like fatigue could be due to anemia, sleep deprivation, a thyroid disorder, or any other myriad conditions that require a diagnostic effort (otherwise known as thinking). And sometimes it's simply done with financial motives, since angiplasty and related procedures pay well.

I call this "drive-by angioplasty," the impulsive, poorly considered coronary procedure that really should never have happened. How often does this happen? What percentage of heart procedures fall into this category? There are no clear-cut estimates. There are crude attempts by independent agencies that have put the number of unnecessary heart catheterizations up to 20% of the total number performed. The proportion of angioplasty procedures, stents, etc. that are not necessary is a tougher number to pinpoint, given the uncertainties surrounding the indications for these procedures, physician judgment that factors into the decision-making process, and the fact that many decisions are made on a qualitative basis, not precise quantification.

In real life, I would put the proportion of flagrant drive-by procedures at no more than 10%. However, that is 10% of an enormous number. The annual cardiovascular healthcare bill is $400 billion. 10% of that is $40 billion--an unimaginable sum. It also adds up to tens of thousands of people per year needlessly subjected to procedures. Consider that 10,000 heart procedures were performed today alone.

Should we push for legislation to control how and when heart procedures are performed? I don't think so. Despite my criticisms of the status quo in heart care, I still favor the freedom and rapid development of a free-market approach. However, you as a healthcare consumer need to be armed with information. You don't go to the car dealer unarmed with information on prices and comparative performance of the car you want. You should do the same with health. Information is your weapon, your defense against becoming the victim of the next drive-by heart procedure.

"Bankers believe liquidation has run its course and advise purchases."

New York Times headline, Oct 30, 1929, at the start of the Great Depression.

"I did not have sexual relations with that woman, Ms Lewinsky."

Former President Bill Clinton at a Washington Press Conference, 1998.

"The third quarter is going to be great."

Enron CEO, Ken Lay, just before the company reported a $638 million third-quarter loss, triggering the company's collapse.

Should we add the following to the list?

Heart Healthy Bisquick

Heart Healthy snacks according to the National Heart, Lung, and Blood Institute:

Animal crackers, devil's food cookies, fig and other fruit bars, ginger snaps, graham crackers, vanilla or lemon wafers

Angel food cake or other lowfat cakes

Low fat frozen yogurt, ice milk, fruit ices, sorbet, sherbet

Pudding (make it with fat free or 1% milk), gelatin desserts

Popcorn without butter or oil; pretzels, baked tortilla chips

67% digestible carbohydrates/sugars from corn syrup, sugar, raisins, and honey. Oh, yes . . . and it contains plant sterols.

"Heartzels are a healthy snack alternative for anyone wanting to control fat intake and add fiber to their diet," said Tracy LaRosiliere, a Frito-Lay vice president of marketing. "What better time for Frito-Lay to launch its first heart-healthy snack than during American Heart Month and just in time for Valentine's Day."

The relationship with the American Heart Association and the launch of Rold Gold Heartzels Pretzels is the latest move by Frito-Lay to continue its commitment to offering a wide variety of low-fat and better-for-you snacks nationally, which like the company's assortment of regular chips can be enjoyed as part of a healthy diet and lifestyle.

Imagine that I'm planning to build a wall of bricks. I start by throwing cement at a pile of bricks, hoping that it forms a nice, orderly brick wall.

Fat chance, you say.

I believe that is what appears to be emerging as the situation with calcium supplementation.

A recent study from New Zealand reported an experience with 1,471 postmenopausal women, mean age of 74 years, who were randomized to treatment with either calcium supplements or placebo. Calcium was supplied as calcium citrate (Citrical) to provide 1000 mg of (elemental) calcium per day (400 mg morning, 600 mg evening).

(Bolland MJ, Barber PA, Doughty RN et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Brit Med J BMJ, doi:10.1136/bmj.39440.525752.BE; published 15 January 2008)

Over 5 years, women taking calcium had twice the risk of having a heart attack compared with women taking the placebo; women taking calcium had a 47 percent higher risk of having any one of three "events" (heart attack, stroke or sudden death) than women in the placebo group.

The findings of this study run counter to what we've been telling people all these years: Calcium supplementation, usually taken to halt deteriorating bone health and osteoporosis, modestly reduces blood pressure, reduces LDL and raises HDL cholesterol. At first blush, we might thereby presume that it also reduces cardiovascular events.

This study suggests that calcium supplementation does not result in reduction of cardiovascular events, perhaps even increases risk.

Certainly, this new finding will serve to confuse the public even more than it is already, particularly when it comes to strategies that modify risk for heart attack. However, this may make more sense once we stop and think for a moment.

Calcium supplementation inarguably slows, occasionally halts, calcium resorption from bone (through suppression of parathyroid hormone). Calcium also accumulates as part of atherosclerotic plaque in coronary and other arteries.

How does oral calcium know where to go--bones, not arteries or kidneys, in addition to serving all its other crucial functions?

Keep in mind that, in many roles, calcium is passive, something that responds to control exerted by some other factor. Vitamin D is that factor. Vitamin D controls the absorption of calcium in the intestinal tract (calcium aborption quadruples when vitamin D is restored to normal), it controls whether calcium is deposited in bone or extracted from arteries. It is the master control over the fate of calcium. Calcium just goes along for the ride.

Bone and arterial health do indeed intersect via calcium, but not through calcium supplementation. Instead, the control exerted by vitamin D (and vitamin K2, another conversation) connects the seemingly unrelated processes.

At what calcium dose threshold do the benefits stop and the adverse effects begin? That remains unanswered, particularly in light of this new study. However, this study calls into serious question the wisdom of supplementing calcium at a dose of 1000 mg, particularly when taken without normalization of vitamin D.

Calcium is therefore emerging as an important player in artery health. But just taking calcium makes no more sense than our brick wall and cement analogy. You might regard vitamin D as the mason that skillfully lays down both brick and cement in a neat, orderly way.

Lorenzo is an 81-year old retired manufacturing engineer whose intial heart scan score in late 2006 was an alarming 1102.

Recall that, despite feeling well and having a normal stress test, Lorenzo was facing a heart attack and death risk that was as high as 25% per year without preventive action.

Lorenzo was moderately interested in the Track Your Plaque concepts. While not exactly the most highly motivated, he did see the rationale in our approach. But he came to us mostly because his primary care doctor told him to.

Nonetheless, one year later, he underwent another heart scan. His score: 588--a 46.6% drop in score, nearly cutting his plaque in half. While Lorenzo didn't set any new records in terms of percentage drop in score, he has reduced his score in real numbers more than anybody else before: a 514 point drop in score.

Lorenzo joins the ranks of our current record holders, Amy, with a 63% drop in heart scan score, and Neal with a 51% drop in score. Both of these Track Your Plaque record holders, while achieving larger percentage reductions in score, achieved less when viewed on an absolute number basis.

Now, breaking records is not necessary to succeed in the Track Your Plaque program or at heart disease reversal. Even 1% reversal is still a big success, certainly more than is achieved in conventional practice.

No special commitment was necessary in Lorenzo's case. All he required was a little of the right kind of information. I can tell what he didn't do: Lorenzo did not follow a low-fat American Heart Association diet, he did not take high-dose statin drug, he did not deprive himself of food, he did not exercise to extremes. He just applied some simple strategies from the Track Your Plaque program.

I play these sorts of games just to make a point and to show just what is possible. While the world of hospital procedures and emergency management of coronary disease marches on, we are quietly reversing the disease. Sometimes, we achieve results that even surprise ourselves.

Lorenzo's full story will be detailed in the February 2008 Track Your Plaque newsletter. If you are not yet a subscriber, you can sign up (without cost)here.

Copyright 2008 William Davis, MD

The conventional answers to high triglycerides levels are generally: low-fat diet, a fibrate drug (Tricor, Lopid), a statin drug, and--most recently--prescription fish oil.

This is the regimen to take if you want the drug industry to get even richer and more powerful than they already are. After all, what CEO of a pharmaceutical company can stand to have his salary and benefits slashed to below $200 million this year? It's outrageous!

If you really want to blast the heck out of your triglycerides and achieve numbers like 50 mg/dl, then the regimen to consider consists of:

--Elimination of sugars, wheat, and cornstarch
--Fish oil--Sam's Club would do fine at $8 for 350 capsules, or the high-potency at $14.99 for 180 capsules (at 680 mg EPA +DHA, nearly the same potency as prescription Lovaza at 842 mg)
--Vitamin D supplementation sufficient to achieve normal blood levels (60-70 ng/ml)

Those three strategies alone can reduce triglycerides far more than any drug combination. In fact, it is rare for someone with triglycerides as high as 900 mg/dl to not reduce them to the <100 mg/dl range.

Followers of The Heart Scan Blog know my feelings about Cheerios:

Can you say "sugar"?

Cheerios and heart health

There's an interesting tussle going on between the makers of Cheerios, General Mills, and the FDA.

The FDA says that the Cheerios' package claims of:

• "you can Lower Your Cholesterol 4% in 6 weeks"
• "Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is ... clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol."

constitute a medical claim, i.e., trying to promote Cheerios as a drug.

I'm glad that the FDA has come down on General Mills. But I find this entire episode laughable: The debate is over the purported health benefits of what I would regard as pure junk food, no better in my view than claiming that a cupcake has health benefits, or a carton of ice cream.

In my experience, Cheerios does not 1) reduce risk for heart disease, nor 2) reduce cholesterol.

It does, however, cause blood sugar to skyrocket and increase the small type of LDL--you know, the type that causes heart disease.

The treatment of angina pectoris, generally speaking, is unsatisfactory.

Any procedure that relieves mental tension is valuable. Since patients suffer particularly during the winter, I encourage winter vacations in a southern climate.

I insist that obese patients lose weight, and have found small doses of benzedrine, 10 to 20 mg. daily, helpful in curbing the appetite.

I generally forbid smoking. This is a particularly disturbing task for many patients to carry out. In such cases, I suggest that 3 or 4 cigarettes be smoked daily, knowing full well that regardless of what I say or recommend, the patients is going to continue to smoke.

Innumerable drugs, most of which are of questionable value, have been used to prevent attacks of angina pectoris. In fact, placebos are frequently of value.

Testosterone--The male sex hormone has been effective in my experience. Whether it acts as a vasodilator or merely by promoting a sense of well-being is not known.

Alcohol--Alcohol (whiskey, brandy, rum) has been used for many years in the treatment of angina pectoris. I have prescribed it in moderate quantity--an ounce several times a day--and while I have not made alcoholics of any of my patients, I also have not cured any of them with it. Preparations, such as creme de menthe, are of value in relieving "gas" of which so many patients complain.

From Heart Disease Diagnosis and Treatment

Emanuel Goldberger, MD

1951

I've noticed a point of confusion recently, something I hadn't noticed in my patients before: Because of the public health advice from the FDA, American Heart Association, and Surgeon General's office to reduce sodium/salt intake, people have thought this meant reducing iodine, too.

I believe that people have drawn an equation in their minds:

Sodium = iodine

Of course, they are two entirely unrelated things.

Recall that the only reason iodine is added to many (not all) salt products is because it was a public health solution to solve the substantial nationwide iodine deficiency prevalent during the 20th century. But it was a solution conceived in 1924, when the FDA thought this was the best way to get iodine into Americans. And it worked.

Unfortunately, sodium does indeed present adverse effects in some people. As a result, "get your iodine from salt" has evolved into "reduce your sodium intake." Everyone forgot about the iodine: They forgot about the large disfiguring goiters, the poor school performance in iodine-deficient schoolchildren, the mentally-impaired offspring of iodine-deficient mothers.

So don't confuse sodium with iodine. You may need less of the former, but more of the latter.

For more on this, see "Help keep your family goiter free."

"I told my cardiologst that I stumbled on a program called 'Track Your Plaque' that claims to be able to help reduce your coronary calcium score.

"My cardiologist said, 'That's impossible. You cannot reduce coronary plaque. I've never seen anyone reduce a heart scan score."

Who's right here?

The commenter is right; the cardiologist is wrong.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Quantify and work to reduce the atherosclerotic plaque? No way! That's work, requires thinking, some sophisticated testing (like lipoprotein testing), even some new ideas like vitamin D. "They didn't teach that to me in medical school (back in 1980)!"

Welcome to the new age.

Atherosclerotic plaque is 1) measurable, 2) trackable, and 3) can be reduced.

We do it all the time. (Amy still holds our record: 63% reduction in plaque/heart scan score.)

Though I pooh-pooh the value of statin drug studies, there's even data from the conventional statin world documenting coronary plaque reversal. The ASTEROID Trial of rosuvastatin (Crestor), 40 mg per day for one year, demonstrated 7% reduction of atherosclerotic plaque using intracoronary ultrasound.

I have NEVER seen a heart attack or appearance of heart symptoms (angina, unstable angina) in a person who has reversed coronary plaque (unless, of course, they pitched the whole effort and returned to bad habits--that has happened). Stick to the program and coronary risk, for all practical purposes, been eliminated.

A heart scan score is not a death sentence. It is simply a tool to empower your prevention program, a measuring stick to gauge plaque progression, stabilization, or regression. Don't accept anything less.

There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself

This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).

If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.

This caught my eye:

Niaspan, prescription niacin, now sold by Abbott Laboratories, is now promoting its advantages in regressing coronary plaque:

In patients with a history of coronary artery disease (CAD) and hypercholesetgerolemia, Niaspan (niacin), in combination with a bile acid-binding resin, is indicated to slow progression or promote regression of atherosclerotic disease.

And the new slogan: "Get regressive."

Interestingly, the new marketing campaign is based on relatively old data. They base this new claim on 3 studies:

1) Cholesterol-Lowering Atherosclerosis Study (CLAS)--a 1987

Lew has coronary plaque with a heart scan score of 393. At age 53, that's in the 90th percentile (higher score than 90% of men in his age group).

On our search for causes of his coronary plaque, we identify low HDL of 41 mg/dl, high triglycerides of 202 mg/dl, small LDL (83% of total), calculated LDL of 133 mg/dl, and severe vitamin D deficiency with a starting blood level of 25-hydroxy vitamin D of 19 ng/ml.

His c-reactive protein: 4.1 mg/dl--above the cut-off of 2.0 mg/dl that the pharmaceutical industry is targeting as a mandate for statin therapy, particularly given the JUPITER data.

Lew instead eliminates wheat and other small LDL-provoking foods and, as a result, loses 28 lbs in 3 months; adds omega-3 fatty acids from fish oil; supplements vitamin D sufficient to increase his blood level to 70 ng/ml.

Along with dramatic correction of his starting abnormalities, his c-reactive protein: 0.4 mg/dl--no statin drug.

In my view, increased CRP is nothing more than a surrogate for the inflammatory phenomena that arise from high-carbohydrate diets, overweight, and small LDL. Correct those and CRP drops off a cliff. In fact, it is exceptionally rare for CRP to not drop to very low levels following this formula.

I believe that CRP is one more item on the list of reasons--the house of cards--the pharmaceutical industry is building to persuade us to take more and more statin drugs. LDL not low enough? Take more statin. Diabetic with low cholesterol? Take a statin. Inflammation? Take a statin.

Enough already.

Our at-home blood tests are proving a hit.

So far, vitamin D is the number one most popular test, no surprise.

Second--to my surprise--is DHEA. I would have predicted it would have been thyroid testing.

Our male and female hormone panels are also proving popular.

I've personally been using the thyroid and vitamin D testing to monitor my levels. I increased my Armour thyroid based on a low free T3 value, while my vitamin D was perfect at 77 ng/ml on 8000 units vitamin D3 (cholecalciferol) per day.

The process of performing the blood spots is straightforward. The finger pricks are virtually painless using the automatic spring-loaded finger stick devices:

The number of blots to make depends on how many tests you'd like. Just a vitamin D test requires 2 blots. If 6 or more tests are ordered at a time, then all 12 blots should be made. (Two spring-loaded lancets are provided in each kit.)

If you are interested in any of our at-home blood tests, go here.

Our own Heart Hawk has posted an editorial on about blood spot testing on Health Central:

Simple, affordable home blood testing is a real game-changer in the arena of informed, self-directed healthcare. For the first time broad access to home blood testing, on a scale similar to that enjoyed by persons who routinely test their blood sugar, is available to virtually everyone and it removes doctors as the gatekeepers of these tests. Even private insurance companies and Medicare are beginning to understand the potential for improving healthcare and decreasing costs and are slowly beginning to expand coverage of home blood testing much as they do for diabetics or persons taking anti-coagulants.

People ask, "If I need iodine, should I go back to iodized salt?"

First of all, how did this notion of iodized salt originate?

In 1924, J. Edgar Hoover was appointed head of the FBI, Marlon Brando and Doris Day were born, and Calvin Coolidge was elected President of the United States. Half of American households had a car, while 1 in 4 Americans were illiterate.

In the 1920s, cities were a fraction of their current size and a third of the U.S. population, or 36 million people, lived in small rural communities.

Goiters were also wildly prevalent in 1924. Up to a third of the population in some areas of the country, particularly the Midwest, suffered from goiters, thyroid glands that enlarged due to lack of iodine.

Goiters were not only unsightly, but sometimes grotesque, causing a visible bulge in the front of the neck. Occasionally, they would grow so big that it compressed adjacent structures, like the trachea, and would have to be surgically removed. Goiters were commonly associated with thyroid dysfunction, especially low thyoid or hypothyroidism, that resulted in low IQ's in schoolchildren, debilitation in adults. Women of childbearing age delivered retarded children.

So iodine deficiency in early 20th century America was a big problem. How to solve this enormous public health problem in a large nation without television, few radios, no internet, with a largely rural and often illiterate population?

Thus was iodized salt born, a simple, technologically available solution that could be implemented on a large scale nationwide at low cost. The FDA chose this route in 1924, figuring that it was the best way to ensure that most Americans could obtain sufficient iodine through liberal use of iodized salt. Public health officials urged Americans to use salt. Morton's salt label proudly bore the slogan "Help keep your family goiter free!"

It worked. Goiters largely became a thing of the past.

How about today? The American Heart Association recommends limiting salt, recently announcing that they would like to limit intake to 1500 mg per day. The American Medical Association has been lobbying the FDA to set lower salt limit guidelines. The FDA has been clamping down on food manufacturers to reduce the quantity of salt in processed foods.

Why limit salt? The concern is that there are segments of the population (not all) that are salt sensitive, particularly African Americans, people with certain genetic forms of high blood pressure, conditions that cause water retention, and any degree of heart or kidney failure. Salt in these peoplem, in fact, can be disastrous.

So adding iodine to salt was the solution to epidemic goiter. And it worked.

But salt is not a perfect solution, just one that served its purpose back in 1924. What we need is a 21st century solution.
You will find that in the various iodine supplements at your health food store. My favorite is kelp--inexpensive, available, and a form that mimics the way Japanese people obtain iodine (though by eating seaweed, rather than with tablets).

Image of kelp courtesy Wikipedia

You can always count on Dr. John Cannell for unique perspectives on vitamin D. I reprint here his unfailingly entertaining and informative Vitamin D Newsletter on whether vitamin D replacement enhances physical performance.

The whole vitamin D "discovery" sometimes worries me. Vitamin D has proven to be an unbelievable, remarkable, dramatic boon to health, including facilitation in dropping CT heart scan scores. Yet the answer was always right in front of us. It worries me that you and I might have the answer to important questions right within our grasp all along--but don't know it. What if the same were true, say, for cancer? That is, a profound answer is right there, but our eyes just pass right over it.

Anyway, we should all keep our eyes open and perhaps you and I will continue to identify the most powerful tools available that return control over heart disease to us and take it away from the perverse, procedural hospital formula that still reigns.

If you haven't done so already, be sure to visit Dr. Cannell's website, www.vitamindcouncil.com.

The Vitamin D Newsletter
March, 2007

Peak Athletic Performance and Vitamin D

"No way doc." I had just finished telling my patient about the benefits of vitamin D, telling him he should take 4,000 IU per day, using all the techniques I had learned in 30 years of medical practice to convince someone proper treatment is important. But, he knew the U.S. government said he only needed 200 IU per day, not 4,000. He also knew the official Upper Limit was 2,000 IU a day. "What are you trying to do doc, kill me?" I told him his 25(OH)-vitamin D blood test was low, only 13 ng/ml. He had read about that too, in a medical textbook, where it said normal levels are between 10 and 40 ng/ml. "I'm fine doc;" adding "Are you in the vitamin business?" I explained I was not; that the government used outdated values; that recent studies indicate ideal 25(OH)D levels are about 50 ng/ml; and that they indicated that he needed about 4,000 IU per day to get his level up to 50. "No thanks doc, I'm fine."

So I tried a different tact. I brought him copies of recent press articles. "Look," I said, "look at these." Science News called vitamin D the Antibiotic Vitamin. The Independent in England says vitamin D explains why people die from influenza in the winter, and not the summer. U.S. News and World Report says almost everyone needs more. Newsweek says it prevents cancer and helps fight infection. In four different recent reports, United Press International says that: it reduces falls in the elderly, many pregnant women are deficient , it reduces stress fractures, and that it helps heals wounds.

He glanced at the articles, showing a little interest in stress fractures. Then he told me what he was really thinking. "Look doc, all this stuff may be important to old guys like you. I'm 22. All I care about are girls and sports. When I get older, maybe I'll think about it. I'm too young to worry about it. I'm in great condition." I couldn't argue. He was in good health and a very good basketball player, playing several hours every day, always on indoor courts.

What could I do to open his eyes? As an African American, his risk of early death was very high, although the risk for blacks doesn't start to dramatically increase until their 40's and 50's. Like all young people, he saw himself as forever young. The U.S. government was no help, relying on a ten-year-old report from the Institute of Medicine that is full of misinformation.

I tired to tell him that the 200 IU per day the U.S. government recommends for 20-year-olds is to prevent bone disease, not to treat low vitamin D levels like his. I pointed out the U.S. government's official current Upper Limit of 2,000 IU/day is the same for a 300 pound adult as it is for a 25 pound toddler. That is, the government says it's safe for a one-year-old, 25-pound, child to take 2,000 IU per day but it's not safe for a 30-year old, 300-pound, adult to take 2,000 and one IU a day. I mean, whoever thought up these Upper Limits must have left their thinking caps at home. Nevertheless, nothing worked. My vitamin D deficient patient was not interested in taking any vitamin D.

What are young men interested in? I remembered that he had told me: "Sex and sports." Two years ago I had researched the medical literature looking for any evidence vitamin D enhanced sexual performance. Absolutely nothing. That would have been nice. Can you imagine the interest?

Then I remembered that several readers had written to ask me if vitamin D could possibly improve their athletic performance? They told me that after taking 2,000 to 5,000 IU per day for several months, they seemed just a little faster, a little stronger, maybe had a little better balance and timing. A pianist had written to tell me she even played a better piano, her fingers moved over the keys more effortlessly! Was vitamin D responsible for these subtle changes or was it a placebo effect? That is, did readers just think their athletic performance improved because they knew vitamin D was a steroid hormone precursor (hormone, from the Greek, meaning "to set in motion")?

The active form of vitamin D is a steroid (actually a seco-steroid) in the same way that testosterone is a steroid and vitamin D is a hormone in the same way that growth hormone is a hormone. Steroid hormones are substances made from cholesterol, which circulate in the body, and work at distant sites by "setting in motion" genetic protein transcription. That is, both vitamin D and testosterone regulate your genome, the stuff of life. While testosterone is a sex steroid hormone, vitamin D is a pleomorphic (multiple function) steroid hormone.

All of a sudden, it didn't seem so silly. Certainly steroids can improve athletic performance although they can be quite dangerous. In addition, few people are deficient in growth hormone or testosterone, so when athletes take sex steroids or growth hormone they are cheating, or doping. The case with vitamin D is quite different because natural vitamin D levels are about 50 ng/ml and, since almost no one has such levels, extra vitamin D is not doping, it's just good treatment. I decided to exhaustively research the medical literature on vitamin D and athletic performance. It took me over a year.

To my surprise, I discovered that there are five totally independent bodies of research that all converge on an inescapable conclusion: vitamin D will improve athletic performance in vitamin D deficient people (and that includes most people). Even more interesting is who published this literature, and when. Are you old enough to remember when the Germans and Russians won every Olympics in the 60's and 70's? Well, it turns out that the most convincing evidence that vitamin D improves athletic performance was published in old German and Russian medical literature.

With the help of my wife and mother-in-law, both of whom are Russian, and with the help of Marc Sorenson, whose book Solar Power is a must read, I finally was able to look at translations of much of the old Russian and German literature. When one combines that old literature with the modern English language literature on neuromuscular performance, the conclusion is inescapable. The readers who wrote me are right.

If you are vitamin D deficient, the medical literature indicates that the right amount of vitamin D will make you faster, stronger, improve your balance and timing, etc. How much it will improve your athletic ability depends on how deficient you are to begin with. How good an athlete you will be depends on your innate ability, training, and dedication. However, peak athletic performance also depends upon the neuromuscular cells in your body and brain having unfettered access to the steroid hormone, activated vitamin D. In addition, how much activated vitamin D is available to your brain, muscle, and nerves depends on having ideal levels of vitamin D in your blood - about 50 ng/ml, to be precise.

Why would I write about such a frivolous topic like peak athletic performance when cancer patients all across this land are dying vitamin D deficient? Like many vitamin D advocates, I have been disappointed that the medical profession and the public don't seem to care about vitamin D. Maybe people, like my young basketball player, will care if it makes better athletes. So, Hey! You jocks! Listen up! I'm talking speed, balance, choice reaction time, muscle mass, muscle strength, squats, reps, etc. Important stuff. Here's the Vitamin D Council's first ever sports quiz.

1. Vitamin D-producing UVB radiation improves athletic performance and may have been widely practiced by German and Russian Olympic athletes in the 1960's and 70's.

True. I found tantalizing evidence the Russians and especially the Germans were on to this during the 60's and 70's when those two nations took turns placing number one and number two in the Olympics every year?

For example, in 1938, Russian researchers reported that a course of ultraviolet irradiations improved speed in the 100-meter dash in college students compared to matched controls, both groups undergoing daily training. Average 100-meter dash times decreased from 13.51 seconds to 13.28 seconds in the non-irradiated controls, but from 13.63 seconds to 12.62 seconds in the irradiated students. Here we see training improved times but training and irradiation improved times much more. Obviously, irradiation or vitamin D would not render the same magnitude of improvements in world-class sprinters, but they would be happy with a few milliseconds.

Gorkin Z, Gorkin MJ, Teslenko NE. [The effect of ultraviolet irradiation upon training for 100m sprint.] The Journal of Physiology of the USSR [Fiziol, z. (RSSR)] 1938; 25: 695-701. (In Russian)

If you want to know what early German thinking was on this, read this summation of the German literature:

"It is a well-known fact that physical performance can be increased through ultra-violet irradiation. In 1927, a heated argument arose after the decision by the German Swimmers' Association to use the sunlamp as an artificial aid, constituting an athletic unfairness, doping, so to speak. In 1926, Rancken had already reported the improving effect of sunlamp irradiation on muscle work with the hand-dynamo-graph. Heib observed an improvement in swimming times after repeated irradiations. In thorough experiments, Backmund showed that a substantial increase in muscle activity happens after radiation of larger portions of the body with an artificial sunlamp; that this performance increase is not caused through local - direct or indirect - effects on the musculature, but through a general effect. This general effect, triggered by ultra-violet irradiation, is caused by a systemic effect on the nervous system." (p. 17)

Parade GW, Otto H. Die beeinflussung der leistungsfahigkeit durch Hohensonnenbestrahlung. Zeitschrift fur Klinische Medizin (Z Klin Med),1940;137:17-21 [In German]

In 1945, two Americans measured the cardiovascular fitness and muscular endurance of 11 male Illinois subjects undergoing training in an indoor physical education class, comparing them to 10 matched controls. Both groups underwent similar physical training. Treatment consisted of ultraviolet irradiation, given in the nude, up to two minutes per session, three times per week, for ten weeks in the late fall and winter. After ten weeks, the treatment group had a 19% standard score gain in cardiovascular fitness compare to a 2% improvement in the control students. To regular readers of this newsletter, it should come as no surprise that the un-irradiated control group reported twice as many viral respiratory infections as the treatment group.

Allen R, Cureton T. Effects of Ultraviolet Radiation on Physical Fitness. Arch Phys Med 1945: 10: 641-44.

In 1952, the German sports medicine researcher, Spellerberg, reported on the effects of wholesale irradiation of athletes studying and training at the Sports College of Cologne - including many elite athletes - with a "central sun lamp." He irradiated the athletes in their bathing suits, on both sides of their bodies, for up to ten minutes, twice a week, for 6 weeks. He reported a "convincing effect" on athletic performance and a 50% reduction in sports injuries. Results were particularly impressive for swimmers, soccer, handball, hockey, and tennis players, as well as for boxers and most track and field athletes. He reported that irradiation leading to burns, further irradiation of athletes having achieved peak performance, and irradiation within 24 hours of competition, all impaired athletic performance. Their results were so convincing, the Sports College of Cologne officially notified the "national German and International Olympic committee." (p. 570)

Spellerberg AE. [Increase of athletic effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 567-70. [In German]

In 1952, Ronge exposed 120 German schoolchildren to UV lights installed in classrooms and compared them to 120 un-irradiated control children. Over a two-year period - excluding summer vacations - he tested both groups with a series of six cardiovascular fitness tests using a bike ergometer. Un-irradiated children showed a distinct seasonality in fitness, with the highest values right after summer break and the lowest values in the spring. Treated children showed no seasonal differences in physical performance. Differences in work performance between the irradiated and un-irradiated children were most conspicuous in the spring with 56% difference between the two groups. In a final experiment, he gave 30 children in the control classrooms 6.25 mg (250,000 IU) of vitamin D as a single dose in February and found their performance had "increased considerably," one month later but did not report the actual numbers. He concluded that vitamin D, either as a supplement or induced via UV irradiation, improved physical performance.

Ronge HE. [Increase of physical effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 563-6. [In German]

In 1954, another researcher, at the Max-Planck Institute for Industrial Physiology in Dortmund, Germany, administered three different wavelengths of UV light over 8 weeks to university students. He found that ultraviolet light in the vitamin D-producing UVB range was consistently effective in reducing resting pulse, lowering the basal metabolic rate, and increasing athletic performance. UVA had no effect; interestingly, artificial UVC irradiation (the atmosphere normally completely filters out UVC radiation and thus it's not naturally present on earth) also gave some positive results.

Lehmann G. [Significance of certain wave lengths for increased efficacy of ultraviolet irradiation.] Strahlentherapie. 1954 Nov;95(3):447-53. [In German]

In 1956, Hettinger and Seidel irradiated seven subjects in two different experiments: athletic performance on bike-ergometers and forearm muscle strength. They found that UV radiation induced a significant improvement in both muscle strength and athletic performance.

Hettinger T, Seidl E. [Ultraviolet irradiation and trainability of musculature.] Internationale Zeitschrift für angewandte Physiologie, einschliesslich Arbeitsphysiologie 1956; 16: 177-83. [In German]

Another German researcher, at the Institute for Medical Physics and Biophysics at the University of Gottiingen, studied reaction times (the time needed to recognize a light and switch it off) during October and November in a series of controlled experiments on 16 children and an unspecified number of adults. He first controlled for practice effects (getting better by practicing) and then administered nine full-body UV radiation treatments over three weeks to the two treatment groups, using placebo radiation in the two control groups. UV radiation improved choice reaction time by 25% in children and 20% in adults while reaction time worsened in controls. The improvements in the irradiated groups peaked at the end of the three weeks of UV treatments and reverted to baseline levels three weeks later. In the two control groups, he found distinctly improved reaction times in the sunnier months.

Sigmund R. [Effect of ultraviolet rays on reaction time in man.] Strahlentherapie. 1956; 101: 623-9. [In German]

The next study threw me because it was very well conducted, meticulously designed, and completely negative. In 1963, Berven reported on the effects of ultraviolet irradiation and vitamin D supplementation in a group of 30 Stockholm schoolchildren, aged 10 -11, comparing them to appropriate controls. He found no seasonality of fitness in the control group and no effect from either irradiation or two different vitamin D supplementation protocols (1500 IU of cholecalciferol daily for two months and a single dose of 400,000 IU of ergocalciferol) on performance on a bike ergometer.

Berven H. The physical working capacity of healthy children; seasonal variations and effect of ultraviolet irradiation and vitamin-D supply. Acta paediatrica. Supplementum 1963; 148: 1-22.

However, two things were not right and got me thinking. One, Berven found no seasonality of physical fitness and was the only author who found no such seasonal variations in athletic performance. Second, he found no effect from irradiation, again, the only author. Then I realized he was working with Swedish children in the late 1950's. Supplementation of children with high doses of vitamin D - often as cod liver oil - was routine in Scandinavia in the past, particularly in children. For example, in neighboring Finland, the official recommended daily dose of vitamin D for children - including infants - was 4,000 IU per day until 1964, when authorities reduced it to 2,000 IU/day. (That's right, you read that correctly, 4,000 IU per day for infants, which is too much by the way.)

In 1975, Finnish authorities reduced it to 1,000 IU per day, and, in 1992, to 400 IU per day. I emailed Professor Elina Hypponen who confirmed that the Swedish recommendations were similar to the Finnish ones. Therefore, it seems highly unlikely that many of Berven's Swedish children, studied in 1958 and 1959, all from "families with a good standard of living," were vitamin D deficient. Therefore, this study showed that vitamin D will not improve athletic ability in vitamin D replete people. That's very important because it indicates more is not necessarily better. More is only better if you are not taking enough.

Hypponen E, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001 Nov 3;358(9292):1500-3.

In the 1960's, three American researchers conducted experiments with university students. Rosentswieg studied the effects of a single six-minute dose of UV light on each side of the trunk in 23 college women, recording changes in various tests of muscle strength at one and five hours. He found a trend towards significance after five hours in white but not African American students. In 1968, Cheatum found that a six-minute administration of UV light, on each side of the trunk, increased the speed of 15 college women in the 30-yard dash. In 1969, Rosentswieg found a six-minute dose of UV light, on each side of the trunk, finding improved performance on a bicycle ergometer in college women. However, unlike the Germans and Russians, I could find no evidence that any of these American findings interested any American professionals involved in the care or training of athletes.

Rosentsweig J. The effect of a single suberythemic biodose of ultraviolet radiation upon the strength of college women. J Assoc Phys Ment Rehabil. 1967 Jul-Aug;21(4):131-3.

Cheatum BA. Effects of a single biodose of ultraviolet radiation upon the speed of college women. Res Q. 1968 Oct;39(3):482-5.

Rosentswieg J. The effect of a single suberythemic biodose of ultraviolet radiation upon the endurance of college women. J Sports Med Phys Fitness. 1969 Jun;9(2):104-6.

2. Athletic performance peaks in the summer when vitamin D levels peak, and is at its lowest in the winter when vitamin D levels are at their lowest.

A. True
B. False

True. The studies below - all I could find in the literature - show tests of physical performance peak in the summer, when vitamin D levels peak, start to decline in early autumn, as vitamin D levels decline, and athletic performance reaches its lowest point in late winter, when vitamin D levels bottom out. However, it is reasonable to assume that any associations between athletic performance and summer season may be due to "reverse causation." That is, improved athletic performance in the summer might be secondary to increased outdoor physical and recreational activity in the warmer weather with an indoor sedentary lifestyle during the colder months. Maybe people have better athletic ability in the summer because they exercise more. If that is true - and using the same logic - athletic performance should not begin to decline until late autumn, because at most temperate latitudes early fall weather is ideal for outdoor physical activities.

However, some of the studies below controlled for seasonal variations in time spent exercising. Furthermore, besides a consistent positive association of summer season with improved athletic performance, the below studies found an abrupt - and unexplained - reduction in athletic performance beginning in the early fall - when vitamin D levels decline - but when the weather is ideal for outdoor activities.

For example, in 1956, German researchers found a distinct seasonal variation in the trainability of musculature, studying wrist flexor strength in 21 German subjects undergoing daily training. They found highly significant seasonal differences with peak performance during the later part of the summer, nadirs in the winter, and an unexplained sharp autumn decline beginning in October.

Hettinger T, Muller EA. Seasonal course of trainability of musculature. Int Z Angew Physiol. 1956;16(2):90-4.

A study of Polish pilots and crew found physical fitness and tolerance to hypoxia were highest in the late summer with an unexplained sharp decline starting in September. The authors hypothesized that seasonal variations in an unidentified hormone best explained their results.

Kwarecki K, Golec L, Klossowski M, Zuzewicz K. Circannual rhythms of physical fitness and tolerance of hypoxic hypoxia. Acta Physiol Pol. 1981 Nov-Dec;32(6):629-36.

Cumulative work ability among 1,835 mainly sedentary Norwegian men during bicycle exercise tests showed an August peak, a sharp decline starting in the autumn, and a wintertime nadir. There were no seasonal changes in body weights, as might be expected if more caloric-demanding recreational activity during the sunnier months explained their results.

Erikssen J, Rodahl K. Seasonal variation in work performance and heart rate response to exercise. A study of 1,835 middle-aged men. Eur J Appl Physiol Occup Physiol. 1979 Oct;42(2):133-40.

Koch and Raschka reviewed the mostly German literature on the seasonality of physical performance, discussing studies indicating that muscle strength and stamina peak in the late summer. The authors then attempted to control for seasonal variations in the time spent exercising by instituting a controlled yearlong training regimen, beginning in December. The training regimen consisted of at least 20 push-ups per day and 2 or 3 long-distances races per week for the entire year. They found the both the number of push-ups and muscle strength peaked in late summer followed by a rapid decline in the fall, and a nadir in the winter, despite continued training. They concluded that seasonal variations in an unidentified hormone best explained their results. In addition, by now we all know that vitamin D is a seasonal hormone, and a steroid hormone precursor to boot.

Koch H, Raschka C. Circannual period of physical performance analysed by means of standard cosinor analysis: a case report. Rom J Physiol. 2000 Jan-Dec;37(1-4):51-8.

3. Vitamin D has direct muscle-building (anabolic) effects.

A. True
B. False

True, but only in vitamin D deficient subjects. Both animal and human studies have found that vitamin D directly affects muscle. That is, vitamin D increases muscle mass.

For example, Birge and Haddad found that vitamin D caused new protein synthesis in rat muscle.

Birge SJ, Haddad JG. 25-hydroxycholecalciferol stimulation of muscle metabolism. J Clin Invest. 1975 Nov;56(5):1100-7.

What about humans? In 1981, Young performed muscle biopsies on 12 severely vitamin D deficient patients before and after vitamin D treatment. They found type-II (fast-twitch) muscle fibers were small before treatment and significantly enlarged after treatment. Sorensen performed muscle biopsies on eleven older patients with osteoporosis before and after treatment with vitamin D. The percentage and area of fast twitch fibers increased significantly after treatment, despite the lack of any physical training.

Young A, Edwards R, Jones D, Brenton D. Quadriceps muscle strength and fibre size during treatment of osteomalacia. In: Stokes IAF (ed) Mechanical factors and the skeleton. 1981. pp 137-145.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Sato reported that two years of treatment with 1,000 IU of vitamin D per day significantly increased muscle strength, doubled the mean diameter, and tripled the percentage of fast-twitch muscle fibers, in the functional limbs of 48 severely vitamin D deficient elderly stroke patients. The placebo control group suffered declines in muscle strength, and in the size and percentage of fast-twitch muscle fibers.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

These studies clearly show that vitamin D when administered to vitamin D deficient people stimulates the growth and number of those muscle fibers critical to athletic ability, type-2, or "fast twitch," muscle fibers.

4. Many studies have found direct associations between physical performance and vitamin D levels. That is, the higher your vitamin D level, the better your athletic performance.

A. True
B. False

True. I found 13 positive studies of associations between vitamin D levels and various parameters of neuromuscular performance. However, they were all in old people. Of course, old people can be athletes too. Furthermore, age differences in physiology and pharmacology are quantitative, not qualitative. That is, what is true in old people will be true in young people, although the magnitude might be different. Higher vitamin D levels are associated with a wide variety of athletic performance but appear to have the strongest associations with balance, timing, and timed tests of physical performance.

The three largest studies had more than 7,000 elderly subjects. All found evidence of a vitamin D threshold of between 30 - 50 ng/ml, above which further improvements in athletic performance were not seen. Wicherts and her colleagues found a linear correlation between vitamin D and neuromuscular performance; scores were 78% better for those with vitamin D levels greater than 30 ng/ml compared to those with levels less than10 ng/ml.

Bischoff-Ferrari HA, Dietrich T, Orav EJ, Hu FB, Zhang Y, Karlson EW, Dawson-Hughes B. Higher 25-hydroxyvitamin D concentrations are associated with better lower-extremity function in both active and inactive persons aged > or =60 y. Am J Clin Nutr. 2004 Sep;80(3):752-8.

Gerdhem P, Ringsberg KA, Obrant KJ, Akesson K. Association between 25-hydroxy vitamin D levels, physical activity, muscle strength and fractures in the prospective population-based OPRA Study of Elderly Women. Osteoporos Int. 2005 Nov;16(11):1425-31.

Wicherts IS, et al. Vitamin D status predicts physical performance and its decline in older persons. J Clin Endocrinol Metab. 2007 Mar 6; [Epub ahead of print]

Professor Heike Bischoff-Ferrari, now in Switzerland, did the largest study. She and her colleagues found a strong positive correlation and suggestion of a U-shaped curve with athletic performance on one test peaking with vitamin D levels of 50 ng/ml but deteriorating at higher levels. It is interesting to speculate that levels around 50 ng/ml may be optimal for athletic performance as such levels are common in humans living in a "natural" state of sun-exposure, such as lifeguards or tropical farmers.

Bischoff HA, Stahelin HB, Urscheler N, Ehrsam R, Vonthein R, Perrig-Chiello P, Tyndall A, Theiler R. Muscle strength in the elderly: its relation to vitamin D metabolites. Arch Phys Med Rehabil. 1999 Jan;80(1):54-8.

Interestingly, all three studies that looked for an association between mental abilities and vitamin D levels found one. A fourth study, unrelated to athletic function, also found an association. The obvious explanation for these findings is that cognitively impaired patients do not go outdoors as often as higher functioning patients and thus have lower vitamin D levels. However, Dhesi found the association after excluding all but mildly demented patients, making such an explanation more difficult. Flicker and - more recently - Przybelski and Binkley, found the association after controlling for outdoor activities, raising the possibility that the association of vitamin D levels with cognitive abilities is casual. Both the vitamin D receptor and the enzyme necessary to activate vitamin D are present in a wide-variety of human brain tissue. If vitamin D deficiency impairs cognitive abilities, it is likely that such deficiencies will also impair the brain's ability to process the complex circuits needed for peak athletic performance.

Dhesi JK, Bearne LM, Moniz C, Hurley MV, Jackson SH, Swift CG, Allain TJ. Neuromuscular and psychomotor function in elderly subjects who fall and the relationship with vitamin D status. J Bone Miner Res. 2002 May;17(5):891-7.

Kenny AM, Biskup B, Robbins B, Marcella G, Burleson JA. Effects of vitamin D supplementation on strength, physical function, and health perception in older, community-dwelling men. J Am Geriatr Soc. 2003 Dec;51(12):1762-7.

Flicker L, Mead K, MacInnis RJ, Nowson C, Scherer S, Stein MS, Thomasx J, Hopper JL, Wark JD. Serum vitamin D and falls in older women in residential care in Australia. J Am Geriatr Soc. 2003 Nov;51(11):1533-8.

Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Jan 8;

There can be no doubt that higher vitamin D levels are associated with improved athletic performance in the elderly. From what we know of physiology and pharmacology, the same associations should hold true in young people, including young athletes.

5. Numerous studies have found that vitamin D improves physical performance.

A. True
B. False.

True, but, again, most all the studies are in old persons, not young ones, and none of the studies are in world-class athletes. However, there is no medical reason why vitamin D would improve the athletic performance of vitamin D deficient old people but not vitamin D deficient young ones. Eleven studies found vitamin D improved physical performance, mainly on measures of balance and reaction time. The one study of younger subjects showed dramatic physical performance effects in 55 severely vitamin D deficient women.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Gloth FM 3rd, Smith CE, Hollis BW, Tobin JD. Functional improvement with vitamin D replenishment in a cohort of frail, vitamin D-deficient older people. J Am Geriatr Soc. 1995 Nov;43(11):1269-71.

Glerup H, Mikkelsen K, Poulsen L, Hass E, Overbeck S, Andersen H, Charles P, Eriksen EF. Hypovitaminosis D myopathy without biochemical signs of osteomalacic bone involvement. Calcif Tissue Int. 2000 Jun;66(6):419-24.

Prabhala A, Garg R, Dandona P. Severe myopathy associated with vitamin D deficiency in western New York. Arch Intern Med. 2000 Apr 24;160(8):1199-203.

Verhaar HJ, Samson MM, Jansen PA, de Vreede PL, Manten JW, Duursma SA. Muscle strength, functional mobility and vitamin D in older women. Aging (Milano). 2000 Dec;12(6):455-60.

Pfeifer M, Begerow B, Minne HW, Abrams C, Nachtigall D, Hansen C. Effects of a short-term vitamin D and calcium supplementation on body sway and secondary hyperparathyroidism in elderly women. J Bone Miner Res. 2000 Jun;15(6):1113-8.

Bischoff HA, Stahelin HB, Dick W, Akos R, Knecht M, Salis C, Nebiker M, Theiler R, Pfeifer M, Begerow B, Lew RA, Conzelmann M. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res. 2003 Feb;18(2):343-51.

Dhesi JK, Jackson SH, Bearne LM, Moniz C, Hurley MV, Swift CG, Allain TJ. Vitamin D supplementation improves neuromuscular function in older people who fall. Age Ageing. 2004 Nov;33(6):589-95.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

In summary, five converging - but totally separate - lines of scientific evidence leave little doubt that vitamin D improves athletic performance. (I actually left out a sixth line of evidence, something a little more complicated, studies of muscle strength and vitamin D receptor polymorphisms; the two studies I could find were both positive.) Anyway, the scientific evidence that UVB radiation, either from the sun or from sunbeds, will improve athletic performance is overwhelming and the mechanism is almost certainly vitamin D production. Peak athletic performance will probably occur with 25(OH)D levels of about 50 ng/ml, whether from sun, sunbeds, or supplements.

All that is missing is a big-time professional or college team identifying and then treating their elite athletes who are vitamin D deficient. Can you imagine what such performance-enhancing effects would do for basketball players, most of who are African American and who practice and play indoors all winter? Or gymnasts? Or weight lifters?

However, a word of caution. The above studies suggest that taking too much vitamin D (more than 5,000 IU per day) may actually worsen athletic performance. Take the right amount, not all you can swallow. Take enough to keep your 25(OH)D levels around 50 ng/ml, year round. Easier yet, regularly use the sun in the summer and sunbeds in the winter - with care not to burn. Once a week should be about right.

When you think about it, none of this should surprise anyone. Every body builder knows that steroid hormones can improve athletic performance, certainly increase muscle mass. Barry Bonds knows they increase timing and power. Moreover, activated vitamin D is as potent a steroid hormone as exists in the human body. However, unlike other steroids, levels of activated vitamin D in muscle and nerve tissue are primarily regulated by sun exposure. That's right, the rate-limiting step for the cellular function (autocrine) of activated vitamin D is under your control. It depends on how much you put in your both or go into the sun. It's ironic that many athletes now avoid the sun, organized baseball is even promoting sun avoidance and sunblocks. The ancient Greeks knew better; they had there elite athletes train on the beach and in the nude.

The medical literature indicates vitamin D levels of about 50 ng/ml are associated with peak athletic performance. Of course, recent studies show such levels are ideal for preventing cancer, diabetes, hypertension, influenza, multiple sclerosis, major depression, cognitive impairments, etc. But who cares about all that disease stuff old people get, we're talking about something really important: speed, balance, reaction time, muscle mass, muscle strength, squats, reps, etc. And guess who's now taking 4,000 IU/day? Yes he is, and he tells me his timing is better, he can jump a little higher, run a little faster, and the ball feels "sweeter," whatever that means.

John Cannell, MD

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. We don't copyright this newsletter. Please feel free to reproduce it and post it on Internet sites and blogs. Remember, we are a non-profit educational organization. Our pathetic finances are available for public inspection. We rely on donations to publish our newsletter and maintain our website. Send your tax-deductible contributions to:

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Atascadero, CA 93422

The reason why I've been blogging lightly these past few days is because, as a favor, I'm covering the practice for some colleagues who I'm (very) loosely affiliated with. The time demands have been great.

Nonetheless, it is a good reminder to me just how far wrong conventional cardiology remains. Judging by what I see around me, there is a startling lack of restraint in proceeding to the catheterization laboratory. Curiously, the internists and family practitioners have been brainwashed into accepting this path. I suppose that all it takes is an occasional real "save" for these physicians to develop a fear of ever missing real disease.

What I'm seeing is just how many people presenting with chest pain or similar symptoms end up going to the cath lab. I would crudely estimate 80%. That is, once you make it past the emergency room, there's a four out of five chance that you'll end up with a heart catheterization to "be sure your heart is okay", "make certain you're not going to die of heart disease", "see if there's a ticking time bomb in your chest". You've heard all the clever, scary phrases that get tossed around to scare the pants off you and justify putting catheters in your groin.

Despite the fact that tools for heart disease prevention have improved dramatically, the volume of heart catheterizations continues to grow nationwide.

I find it shocking and unacceptable. We're currently working behind the scenes to help change this situation through education of the public. Persuade a $1 million a year cardiologist that he is overdoing procedures? Unlikely in my experience. Educate the public about the shocking over-reliance on high-revenue procedures? Perhaps more practical.

Garlic May Not Lower Cholesterol
Study Shows No Improvement in Cholesterol Levels From Raw Garlic or Garlic Supplements

Lots of reports continue to hit the press about a small study that hoped to determine whether garlic as whole cloves (4 to 6), an aqueous extract of garlic called Kyolic, or an oil extract called Garlicin (high in allicin), or placebo. No differences in lipid numbers including LDL cholesterol were observed.

(Full text at WebMD at http://www.webmd.com/cholesterol-management/news/20070226/garlic-may-not-lower-cholesterol?ecd=wnl_chl_030507. You may be required to log in or register.)

I believe that the researchers were sincere in their effort to follow an honest, scientfically sound clinical trial design. I'm personally not that surprised. The effect in prior studies has been modest, sometimes none. Does that mean that we should ignore the other studies that suggest there may be modest blood-thinning, anti-inflammatory, blood pressure-reducing, and cancer-preventing properties? No, it does not. Dr. Matt Budoff at UCLA even published a very small study in about 20 people that suggested a slowing of plaque growth by using Kyolic in persons tracked by CT heart scans.

Nonetheless, garlic is, at best, probably no more than a source of small benefits. The biggest fallout from this kind of report, however, is not the neutral results from garlic, but from the open door the drug companies sense when this happens.

If you read the WebMD report, you'll notice all sorts of advertisements from drug companies for statin cholesterol drugs ("Cholesterol health center"; "Understanding Cholesterol Numbers"; "There are two sources of cholesterol: food and family"), Niaspan (which I used to support but have been discouraged by the Kos companies excessively profiteering methods and recent big Wall Street sellout).

It doesn't follow. The failure of one nutritional strategy to reduce LDL does nothave to trigger a run to the drugs. Don't fall for it. Drugs have their place. So do supplements and food choices, which can be very powerful. Drug manufacturers and their marketing people salivate when something like this comes along, an open invitation to say, "If garlic doesn't work, _____ sure does."

Jason came to the office because of chest pain. At 34 years old, he works as manager of a (non-fast food) restaurant, but indulges in lots of the odds and ends. Among his indulgences: Diet Coke.

Every time he'd have a diet Coke, he'd have chest pain. Not drinking diet Coke--no chest pain. If Jason drank coffee, no chest pain. Other foods, no chest pain. Anyway, just eliminating the diet Coke seemed to do the trick. (Aspartame?)

Anyway, that's not why I tell you Jason's story. In the midst of his evaluation, an echocardiogram showed a mildly enlarged aorta, measuring 4.0 cm in diameter. So we obtained lipoproteins. Jason showed lipoprotein(a) and small LDL particles, the dreaded duo. We talked about how to correct this pattern. Among the strategies we discussed was niacin.

But what bothered me was that neither of Jason's parents had a diagnosis of heart disease. Jason had to have gotten Lp(a) from either his mother or father, since you obtain the gene from one or the other parent. You cannot acquire Lp(a). So one of Jason's parents was sitting on a genetic time bomb of unrecognized Lp(a) and hidden heart disease.

Because Jason's paternal grandfather had a heart attack at age 62, only Jason's Dad had the heart scan (though I urged both to get one). Score: 1483. Recall that heart scan scores >1000 carry a risk of death or heart attack of 25% per year if no preventive action is taken. Now, of course, we have to persuade Jason's Dad that a program of prevention--intensive prevention is in order, including a measure of Lp(a).

So that's the curious story of how Diet Coke probably saved Jason's Dad's life. The lesson is that if you or someone you know has Lp(a), think about their children as well as their parents, each of whom carry a 50% chance of having the pattern.

There's a widely-known (among cardiologists) problem with nuclear stress tests. It's called the "false positive." (Nuclear stress tests are known as stress Cardiolites, stress thalliums, stress Myoviews, persantine stress tests, adenosine stress tests)

Stress tests, nuclear and otherwise, are helpful for identifying areas of poor blood flow. If an area of poor blood flow is detected and the area is substantial, then there may be greater risk of heart attack and other undesirable events in the relatively near future.

What "false positive" means is a stress test that shows an abnormality but it's not true--it is falsely abnormal. There are a number of reasons why this can happen. The problem is that this phenomenon is very common. Up to 20% of nuclear stress tests are false positives.

There are indeed situations where there may an abnormality and it is not clear whether it is true or false. This may lead to a justifiable heart catheterization or CT coronary angiogram. But, given the extraordinary number of false positives, there's a lot of gray in interpreting these tests. Hospital staff, in fact, call nuclear medicine "unclear" medicine. It's common knowledge that you can often see just about anything you want to see on a nuclear image of the heart. Abnormalities in the bottom of the heart, the "inferior" wall, are especially common due to the overlap of the diaphragm with the heart muscle, yielding the appearance of reduced blood flow. Defects in the front of the heart heart are common in females with large breasts for the same reasons.

The problem: The uncertainty inherent in nuclear stress tests opens the door to the unscrupulous or lazy practitioner. Any blip, tick, or imperfection on the nuclear images serve as carte blanche to drag you into the hospital for procedures.

This abusive practice is, in my experience, shockingly common for two reasons: 1) It pays better to do heart catheterizations, and 2) Defensive medicine.

What's the disincentive? Only doing the right thing and maintaining a clear conscience. Slim reasons for many of my colleagues--and a lot less money.

If you are without symptoms and feel fine, and a nuclear stress test is advised by your doctor, followed by a discussion of an abnormality, insist on a discussion of exactly what is abnormal, just how abnormal, and what the alternatives might be. If you receive unsatisfactory or incomplete answers despite your best effort, it's time for another opinion.

Magnesium is kind of boring. So most people don't pay too much attention to it.

Magnesium can be important, however. I saw an interesting phenomenon recently. A type I diabetic patient of mine (that is, an adult who developed diabetes as a child), Mitch, was experiencing wide swings in blood sugar: low low's and very high high's (300-400 mg/dl). Mitch's magnesium was only marginally low at 2.0 mEq/L. (Ranges for normal magnesium blood levels are usually 1.3–2.1 mEq/L or 0.65–1.05 mmol/L.) Note that Mitch's blood levels fall within "normal." I do not agree with these "normal" ranges. I shoot for 2.1 to 2.4 mEq/L, which I think is the truly normal range.

In addition to eating plenty of raw nuts and green vegetables, Mitch began supplementing magnesium with magnesium citrate, 200 mg twice a day (our preferred supplement form). He reported that the wide swings in blood sugar were nearly eliminated.

Mitch's dramatic benefit is just a great illustration of how magnesium can help control blood sugar metabolism. A type I diabetic is more sensitive to the effects, but anyone with type II (adult) diabetes, metabolic syndrome, or just a slightly high blood sugar could benefit from magnesium supplementation.

There's a number of ways to accomplish getting sufficient magnesium in your daily regimen. Track Your Plaque members, Be sure to read:

Your water may be killing you at
http://www.cureality.com/library/fl_03-002magnesium.asp

Magnesium: Water to the rescue! at http://www.cureality.com/library/fl_03-010magnesium2.asp

It struck me recently that, for many people, it's not the second but the third heart scan that more commonly shows a reduction in score.

I think this is because many people's reaction to their first heart scan is "This can't be. There's no way my arteries have that much plaque." They then follow a half-hearted program to correct their patterns.

When the second heart scan shows a significantly higher score, that really catches their attention. This is when they finally buckle down and give it their all.

Only the occasional person will, after the first heart scan, seize full control and take their program very seriously. These tend to be highly motivated people.

Don't feel too bad if your second heart scan score shows an increase. Look at it for what it represents: feedback on the adequacy of your program.

Peter started out at age 59 at 248 lbs, standing 6 ft tall (BMI = 33.6!).

Along with his weight, Peter had the entire panel of phenemena of the so-called "metabolic syndrome", or pre-diabetes:

--Triglycerides 238 mg/dl and associated with extremes of excess VLDL and IDL
--High blood pressure
--Blood sugar 115 mg/dl
--High c-reactive protein
--Small LDL particles 99% of total LDL

Interestingly, Peter's HDL was a surprisingly favorable 58 mg/dl (HDL is usually low in this syndrome). However, when broken down by size, he had nearly zero large, healthy HDL (sometimes called HDL2b). Though total HDL was favorable, most of it was simply ineffective.

Peter eliminated snacks and processed foods, particularly bread; increased his reliance on healthy oils and lean proteins; incorporated soy protein; increased vegetables. He added 30 minutes of a rapid walk on a treadmill every day. He added vitamin D to achieve a blood level of 50 ng/dml. He added a magnesium supplement.

Peter has lost 31 lbs. in the last year. Weight 207 lbs., BMI 28.1 (desirable <25). Blood sugar: 96 mg/dl; triglycerides: 56 mg/dl; HDL 71 mg/dl with 35% in the large fraction; small LDL 45% of total. Not perfect, but a damn site better.

Control of metabolic syndrome is an achievable goal for over 90% of people, just with these simple efforts. We haven't yet had a chance to assess the effect on the progression or regression of Peter's heart scan score, but he has, at the very least, spared himself a future of diabetes and all its complications.

This is a "slice" from a normal heart scan in a 58 year old woman. Heart scan score zero. Look at the lungs, the dark areas left and right of the heart in the center. The lungs are also normal. Black represents normal density, healthy lung tissue. The white streaking is just normal lung blood vessels. This person doesn't smoke.

This woman smokes a pack of cigarettes a day and has done so for 45 years ("45 pack-years"). She had a surprisingly low heart scan score (at age 64) of only 71, despite the smoking. However, look at this woman's lungs. It's a little tough to make out, since the computer graphics loses some of the resolution. But you can see the near absence of lung tissue on both sides. This is an advanced phase of the destructive lung disease, emphysema, from smoking. Even if she quit smoking today, the destroyed lung tissue never grows back. She literally has huge gaps or holes in her lungs where lung tissue used to be.

Smoking is among the most destructive, terrible things you can do to your body, short of swallowing strychnine or jumping off a building. Stay as far the heck away from cigarettes as you possibly can. If you are exposed to "secondary" smoke, insist that the person never smoke in your presence. It's not the smell that destroys your lungs or causes coronary plaque (though it is indeed foul), it's the actual smoke.

Do you need to become a vegetarian in order to reduce your heart scan score?

No. Plain and simple. We’ve had many non-vegetarians drop their scores.

That said, are there still advantages to following a vegetarian diet, or some variation on the vegetarian theme?

Yes, there are. Let’s put aside the moral or religious arguments in favor of not eating animals—the need to eliminate killing animals for food, elimination of suffering common in modern livestock practices, Kosher considerations, etc. (Not that there aren’t real arguments here. Our focus for this conversation is not, however, the moral dilemma, but the health argument.)

Some of the most unhealthy people I’ve ever met, mostly males, are proud carnivores who boast of their prodigious capacities to eat meat. Unfortunately, it’s hard to tease out the ill-effects of excessive meat eating, since these same men also tend to be substantially overweight, smoke, drink excessively, and fail to get exercise unless their job is physically demanding. You know the type.

What advantages does a vegetarian obtain? A number of studies have suggested that the reduced saturated fat, reduced exposure to parasites, as well as reduced exposure to the antibiotics and hormones now used routinely in livestock-raising practices, do indeed provide benefits to the vegetarian. Thus, vegetarians tend to be substantially thinner, experience less bowel cancer, have less diabetes and heart disease, and live longer.

(If you are interested in reading or seeing more about just how inhumane modern livestock practices are, take a look at the video, "Meet Your Meat" at meat.org. Be sure not to view this after dinner.)

Of course, some of the disadvantages of eating animal products diminish when free-range livestock are eaten, i.e., livestock not raised in the inhumane cramped, filthy conditions of livestock factories, but in the open, grazing or rooting freely. These animals tend to have different fat compositions and taste different.

The advantages of vegetarianism, however, have blurred in recent years, since many so-called vegetarians have failed to maintain the distinction between naturally-occurring foods and processed foods. So, Ritz Crackers, Oreo cookies, whole wheat bread, and Raisin Bran fit into a vegetarian program, but they’re awful for your health. I’ll occasionally meet a self-proclaimed vegetarian who looks every bit as unhealthy as a conventionally eating American, that is, overweight, pre-diabetic person with a developing heart scan score.

So it is not necessary to be vegetarian to reduce your score. You might consider vegetarianism for other reasons, such as moral considerations, or to reduce your risk for cancer. But it is not necessary to drop your heart scan score. A non-processed food diet? Now that's is worth giving serious consideration.